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<title>Toxicology and Industrial Health</title>
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<title><![CDATA[Mold and mycotoxin symposium: Towards healthy homes]]></title>
<link>http://tih.sagepub.com/cgi/reprint/25/9-10/569?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Kilburn, K. H]]></dc:creator>
<dc:date>Fri, 23 Oct 2009 04:11:59 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709348259</dc:identifier>
<dc:title><![CDATA[Mold and mycotoxin symposium: Towards healthy homes]]></dc:title>
<prism:number>9-10</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>569</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>569</prism:startingPage>
<prism:section>Articles</prism:section>
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<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/9-10/571?rss=1">
<title><![CDATA[Epidemics of mold poisoning past and present]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/9-10/571?rss=1</link>
<description><![CDATA[<p>Molds are ubiquitous throughout the biosphere of planet earth and cause infectious, allergic, and toxic diseases. Toxic diseases arise from exposure to mycotoxins produced by molds. Throughout history, there have been a number of toxic epidemics associated with exposure to mycotoxins. Acute epidemics of ergotism are caused by consumption of grain infested by fungi of the genus Claviceps, which produce the bioactive amine ergotamine that mimics the neurotransmitters norepinephrine, serotonin, and dopamine. Acute aflatoxin outbreaks have occurred from ingestion of corn stored in damp conditions that potentiate growth of the molds of the species Aspergillus. Contemporary construction methods that use cellulose substrates such as fiber board and indoor moisture have caused an outbreak of contaminated buildings with Stachybotrys chartarum, with the extent of health effects still a subject of debate and ongoing research. This article reviews several of the more prominent epidemics and discusses the nature of the toxins. Two diseases that were leading causes of childhood mortality in England in the 1970s and vanished with changing dietary habits, putrid malignant fever, and slow nervous fever were most likely toxic mold epidemics.</p>]]></description>
<dc:creator><![CDATA[Meggs, W. J]]></dc:creator>
<dc:date>Fri, 23 Oct 2009 04:11:59 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709348277</dc:identifier>
<dc:title><![CDATA[Epidemics of mold poisoning past and present]]></dc:title>
<prism:number>9-10</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>576</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>571</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/9-10/577?rss=1">
<title><![CDATA[Neurologic and neuropsychiatric syndrome features of mold and mycotoxin exposure]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/9-10/577?rss=1</link>
<description><![CDATA[<p>Human exposure to molds, mycotoxins, and water-damaged buildings can cause neurologic and neuropsychiatric signs and symptoms. Many of these clinical features can partly mimic or be similar to classic neurologic disorders including pain syndromes, movement disorders, delirium, dementia, and disorders of balance and coordination. In this article, the author delineates the signs and symptoms of a syndrome precipitated by mold and mycotoxin exposure and contrasts and separates these findings neurodiagnostically from known neurologic diseases. This clinical process is designed to further the scientific exploration of the underlying neuropathophysiologic processes and to promote better understanding of effects of mold/mycotoxin/water-damaged buildings on the human nervous system and diseases of the nervous system. It is clear that mycotoxins can affect sensitive individuals, and possibly accelerate underlying neurologic/pathologic processes, but it is crucial to separate known neurologic and neuropsychiatric disorders from mycotoxin effects in order to study it properly.</p>]]></description>
<dc:creator><![CDATA[Empting, L.]]></dc:creator>
<dc:date>Fri, 23 Oct 2009 04:11:59 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709348393</dc:identifier>
<dc:title><![CDATA[Neurologic and neuropsychiatric syndrome features of mold and mycotoxin exposure]]></dc:title>
<prism:number>9-10</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>581</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>577</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/9-10/583?rss=1">
<title><![CDATA[The biocontaminants and complexity of damp indoor spaces: more than what meets the eyes]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/9-10/583?rss=1</link>
<description><![CDATA[<p>Nine types of biocontaminants in damp indoor environments from microbial growth are discussed: (1) indicator molds; (2) Gram negative and positive bacteria; (3) microbial particulates; (4) mycotoxins; (5) volatile organic compounds, both microbial (MVOCs) and non-microbial (VOCs); (6) proteins; (7) galactomannans; (8) 1-3-&beta;-D-glucans (glucans) and (9) lipopolysaccharides (LPS &mdash; endotoxins). When mold species exceed those outdoors contamination is deduced. Gram negative bacterial endotoxins, LPS in indoor environments, synergize with mycotoxins. The gram positive Bacillus species, Actinomycetes (Streptomyces, Nocardia and Mycobacterium), produce exotoxins. The Actinomycetes are associated with hypersensitivity pneumonitis, lung and invasive infections. Mycobacterial mycobacterium infections not from M. tuberculosis are increasing in immunocompetent individuals. In animal models, LPS enhance the toxicity of roridin A, satratoxins G and aflatoxin B1 to damage the olfactory epithelium, tract and bulbs (roridin A, satratoxin G) and liver (aflatoxin B1). Aflatoxin B1 and probably trichothecenes are transported along the olfactory tract to the temporal lobe. Co-cultured Streptomyces californicus and Stachybotrys chartarum produce a cytotoxin similar to doxorubicin and actinomycin D (chemotherapeutic agents). Trichothecenes, aflatoxins, gliotoxin and other mycotoxins are found in dust, bulk samples, air and ventilation systems of infested buildings. Macrocyclic trichothecenes are present in airborne particles &lt;2 &micro;m. Trichothecenes and stachylysin are present in the sera of individuals exposed to S. chartarum in contaminated indoor environments. Haemolysins are produced by S. chartarum, Memnoniella echinata and several species of Aspergillus and Penicillium. Galactomannans, glucans and LPS are upper and lower respiratory tract irritants. Gliotoxin, an immunosuppressive mycotoxin, was identified in the lung secretions and sera of cancer patients with aspergillosis produced by A. fumigatus, A. terreus, A. niger and A. flavus.</p>]]></description>
<dc:creator><![CDATA[Thrasher, J. D, Crawley, S.]]></dc:creator>
<dc:date>Fri, 23 Oct 2009 04:12:00 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709348386</dc:identifier>
<dc:title><![CDATA[The biocontaminants and complexity of damp indoor spaces: more than what meets the eyes]]></dc:title>
<prism:number>9-10</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>615</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>583</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/9-10/617?rss=1">
<title><![CDATA[Molds, mycotoxins, and sick building syndrome]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/9-10/617?rss=1</link>
<description><![CDATA[<p>The following is a review of some of the work we have done since 2004 regarding the importance of molds and their mycotoxins in the phenomenon of sick building syndrome (SBS). In these studies we showed that the macrocyclic trichothecene mycotoxins (MTM) of Stachybotrys chartarum (SC) are easily dissociated from the surface of the organism as it grows and could therefore be consequently spread in buildings as the fungus experiences additional water events. We then showed that SC and Penicillium chrysogenum (PC) colonies remain viable long after a water source has been removed, and the MTM produced by SC remain toxic over extended periods of time. We next showed that PC when inhaled, can release in vivo, a protease allergen that can cause a significant allergic inflammatory reaction in the lungs of mice. We then showed, in a laboratory study, that the MTM of SC can become airborne attached to spores or SC particulates smaller than spores. Following that study, we next showed that the same phenomenon actually occurred in SC infested buildings where people were complaining of health problems potentially associated with SBS. Finally, we were able to demonstrate the presence of MTM in the sera of individuals who had been exposed to SC in indoor environments. This last study was done with enough mold exposed individuals to allow for the statistical significance of SC exposure to be evaluated.</p>]]></description>
<dc:creator><![CDATA[Straus, D. C]]></dc:creator>
<dc:date>Fri, 23 Oct 2009 04:12:00 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709348287</dc:identifier>
<dc:title><![CDATA[Molds, mycotoxins, and sick building syndrome]]></dc:title>
<prism:number>9-10</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>635</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>617</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/9-10/637?rss=1">
<title><![CDATA[Mycotoxins in animal and human patients]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/9-10/637?rss=1</link>
<description><![CDATA[<p>The majority of human food and animal feed production occurs in a highly managed agroecosystem. Management decisions include variety grown, tillage and irrigation methods and practices, fertilization, pest and disease control, harvesting methods, and storage and transportation practices. This system is generally managed for optimum returns to labor and capital investments. The spores of toxigenic fungi have ubiquitous distribution and toxigenic fungi exploit food sources when conditions of moisture and temperature are above minimums for growth. The safety margins in the agroecosystem are close and are influenced by extrinsic factors such as climatic events. Control of fungal growth is important in management of raw feedstuffs, foodstuffs, condiments-spices, botanicals, and other consumable substances as they are grown, harvested, stored, and transported. The risk factors for mycotoxin production are weather conditions during crop growth and when the crop is mature, damage to seeds before, during, and after harvest, how commodities are physically handled, the presence of weed seeds and other foreign material in grain, and how commodity moisture and temperature are managed during storage and transportation. Diversion of commodities and by-products from human consumption to animal feedstuffs can increase the risk of mycotoxicoses in animals. The toxicology of selected toxigenic fungi and the mycotoxins they produce are reviewed.</p>]]></description>
<dc:creator><![CDATA[Coppock, R. W, Jacobsen, B. J]]></dc:creator>
<dc:date>Fri, 23 Oct 2009 04:12:00 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709348263</dc:identifier>
<dc:title><![CDATA[Mycotoxins in animal and human patients]]></dc:title>
<prism:number>9-10</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>655</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>637</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/9-10/657?rss=1">
<title><![CDATA[Health effects of Aspergillus in food and air]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/9-10/657?rss=1</link>
<description><![CDATA[<p>This review summarizes the health aspects of the medically important fungal genus Aspergillus. The morphology and systematics of the genus are explained as well as its biogeography. Major mycotoxins, the aspergilli that produce them, affected crops, and symptoms of the toxicoses are summarized, as are the major mycoses caused by aspergilli. The current status of the relationship between Aspergillus in the indoor environment and health issues are discussed.</p>]]></description>
<dc:creator><![CDATA[Klich, M. A]]></dc:creator>
<dc:date>Fri, 23 Oct 2009 04:12:00 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709348271</dc:identifier>
<dc:title><![CDATA[Health effects of Aspergillus in food and air]]></dc:title>
<prism:number>9-10</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>667</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>657</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/9-10/669?rss=1">
<title><![CDATA[Fungal exposure endocrinopathy in sinusitis with growth hormone deficiency: Dennis-Robertson syndrome]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/9-10/669?rss=1</link>
<description><![CDATA[<p>A retrospective study was carried out on 79 patients with a history of mold exposure, fatigue, and chronic rhinosinusitis (CRS) to determine whether there is a causal relationship between fungal exposure and chronic sinusitis, fatigue, and anterior hypopituitarism, especially growth hormone deficiency (GHD). Of the patients, 94% had a history of CRS, endoscopically and/or computed tomography (CT) confirmed; 100% had chronic fatigue and 100% had either significant history of indoor mold exposure and/or positive mold plate testing as measured by settle plates, with an average colony count of 21 (0-4 normal). A total of 62 had positive mold plate testing and 17 had positive history of mold exposure. Of 75, 73 (97.3%) had positive serum immunoglobulin G (IgG)-specific antibodies to fungal antigens. Out of 8, 7 were positive for urinary trichothecenes. Resting levels of insulin-like growth factor 1 (IGF-1) averaged 123 ng/mL (range 43-285, normal 88-249 ng/mL). Despite normal resting levels of IGF-1, significant deficiency of serum human growth hormone (GH) was confirmed by insulin tolerance test (ITT) in 40 of 50 tested. In all, 51% (40/79) were GH deficient. Primary or secondary hypothyroidism in T3 and/or T4 was seen in 81% (64/79) patients; 75% (59/79) had adrenocorticotrophic hormone (ACTH) deficiency. Fungal exposure endocrinopathy likely represents the major cause of GHD, affecting approximately 4.8 million people compared to approximately known 60,000 cases from all other causes. A literature review indicates a possible mechanism of GHD in fungal exposure is that the fungal glucan receptors in the lenticulostellate cells of the anterior pituitary bind to fungal cells wall glucans and activate the innate immune system, which activates macrophages that destroy the fungus and lenticulostellate tissue. Treatment of patients included normal saline nasal irrigations, antifungal and antibiotic nasal sprays, appropriate use of oral antibiotics and antifungals, facial steamer with CitriDrops. Thymate and/or Intramax vitamin supplements, hormone replacement, and reduction of indoor mold levels. Resolution of rhinosinusitis was seen in 93% (41 of 45) of the patients who achieved a mold count by settling plates of 0-4 colonies. Thirty patients were unable to lower their mold counts below four colonies and had various degrees of mucosal disease and fatigue remaining. Fatigue was improved in all 37 patients who received GH and cortisol and/or thyroid hormone, which were deficient. Fatigue was partially relieved in 7 of the 37 who did not achieve mold counts of fewer than four colonies.</p>]]></description>
<dc:creator><![CDATA[Dennis, D., Robertson, D., Curtis, L., Black, J.]]></dc:creator>
<dc:date>Fri, 23 Oct 2009 04:12:00 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709348266</dc:identifier>
<dc:title><![CDATA[Fungal exposure endocrinopathy in sinusitis with growth hormone deficiency: Dennis-Robertson syndrome]]></dc:title>
<prism:number>9-10</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>680</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>669</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/9-10/681?rss=1">
<title><![CDATA[Neurobehavioral and pulmonary impairment in 105 adults with indoor exposure to molds compared to 100 exposed to chemicals]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/9-10/681?rss=1</link>
<description><![CDATA[<p>Patients exposed at home to molds and mycotoxins and those exposed to chemicals (CE) have many similar symptoms of eye, nose, and throat irritation and poor memory, concentration, and other neurobehavioral dysfunctions. To compare the neurobehavioral and pulmonary impairments associated with indoor exposures to mold and to chemicals. 105 consecutive adults exposed to molds (ME) indoors at home and 100 patients exposed to other chemicals were compared to 202 community referents without mold or chemical exposure. To assess brain functions, we measured 26 neurobehavioral functions. Medical and exposure histories, mood states score, and symptoms frequencies were obtained. Vital capacity and flows were measured by spirometry. Groups were compared by analysis of variance (ANOVA) after adjusting for age, educational attainment, and sex, by calculating predicted values (observed/predicted <FONT FACE="arial,helvetica">x</FONT> 100 = % predicted). And p &lt; .05 indicated statistical significance for total abnormalities, and test scores that were outside the confidence limits of the mean of the percentage predicted. People exposed to mold had a total of 6.1 abnormalities and those exposed to chemicals had 7.1 compared to 1.2 abnormalities in referents. Compared to referents, the exposed groups had balance decreased, longer reaction times, and blink reflex latentcies lengthened. Also, color discrimination errors were increased and visual field performances and grip strengths were reduced. The cognitive and memory performance measures were abnormal in both exposed groups. Culture Fair scores, digit symbol substitution, immediate and delayed verbal recall, picture completion, and information were reduced. Times for peg-placement and trail making A and B were increased. One difference was that chemically exposed patients had excess fingertip number writing errors, but the mold-exposed did not. Mood State scores and symptom frequencies were greater in both exposed groups than in referents. Vital capacities were reduced in both groups. Neurobehavioral and pulmonary impairments associated with exposures to indoor molds and mycotoxins were not different from those with various chemical exposures.</p>]]></description>
<dc:creator><![CDATA[Kilburn, K. H]]></dc:creator>
<dc:date>Fri, 23 Oct 2009 04:12:00 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709348390</dc:identifier>
<dc:title><![CDATA[Neurobehavioral and pulmonary impairment in 105 adults with indoor exposure to molds compared to 100 exposed to chemicals]]></dc:title>
<prism:number>9-10</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>692</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>681</prism:startingPage>
<prism:section>Articles</prism:section>
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<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/9-10/693?rss=1">
<title><![CDATA[Detection of macrocyclic trichothecene mycotoxin in a caprine (goat) tracheal instillation model]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/9-10/693?rss=1</link>
<description><![CDATA[<p>This study demonstrates the detection and dynamics of macrocyclic trichothecene mycotoxin (MTM) tissue loading using a commercially available assay in a goat model. The detection of MTMs has been difficult and complex due to the uncertainty of what tissues to examine and when to sample. Twelve goats (two groups of each) were instilled with Stachybotrys chartarum conidial suspension via the trachea. The first group was challenged repeatedly with fungal conidia containing 1 mg/kg of MTM per instillation whereas the second group was exposed once, to spores with a calculated concentration of 5 &micro;g/kg of mycotoxin. These toxin estimates were generated by the QuantiTox<sup>TM</sup> Kit assay; a conidium of S. chartarum possessed 8.5 pg of MTM. After repeated exposure of 3 days, MTM was detected in one of six animals. This animal and two others from the same group had mycotoxin detected in their serum 24 hours after challenge at a comparable level (1.69 ng/mL) to the six animals challenged with a single dose (2.02 ng/mL) at the same time post-instillation. Results showed that MTMs are detectable in experimental animals soon after challenge and contribute to the understanding of the role of these mycotoxins in the disease process following mold exposure.</p>]]></description>
<dc:creator><![CDATA[Layton, R. C, Purdy, C. W, Jumper, C. A, Straus, D. C]]></dc:creator>
<dc:date>Fri, 23 Oct 2009 04:12:00 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709348275</dc:identifier>
<dc:title><![CDATA[Detection of macrocyclic trichothecene mycotoxin in a caprine (goat) tracheal instillation model]]></dc:title>
<prism:number>9-10</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>701</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>693</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/9-10/703?rss=1">
<title><![CDATA[Do terbutaline- and mold-associated impairments of the brain and lung relate to autism?]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/9-10/703?rss=1</link>
<description><![CDATA[<p>Increased prevalence of the autism spectrum disorders (ASD) and the failure to find genetic explanations has pushed the hunt for environmental causes. These disorders are defined clinically but lack objective characterization. To meet this need, we measured neurobehavioral and pulmonary functions in eight ASD boys aged 8 to 19 years diagnosed clinically and compared them to 145 unaffected children from a community with no known chemical exposures. As 6 of 35 consecutive mold/mycotoxin (mold)-exposed children aged 5 to 13 years had ASD, we compared them to the 29 non-ASD mold-exposed children, and to the eight ASD boys. Comparisons were adjusted for age, height, weight, and grade attained in school. The eight ASD boys averaged 6.8 abnormalities compared to 1.0 in community control boys. The six mold-exposed ASD children averaged 12.2 abnormalities. The most frequent abnormality in both groups was balance, followed by visual field quadrants, and then prolonged blink reflex latency. Neuropsychological abnormalities were more frequent in mold-exposed than in terbutaline-exposed children and included digit symbol substitution, peg placement, fingertip number writing errors, and picture completion. Profile of mood status scores averaged 26.8 in terbutaline-exposed, 52 in mold exposed, and 26 in unexposed. The mean frequencies of 35 symptoms were 4.7 in terbutaline, 5.4 in mold/mycotoxins exposed and 1.7 in community controls.</p>]]></description>
<dc:creator><![CDATA[Kilburn, K. H, Thrasher, J. D, Immers, N. B]]></dc:creator>
<dc:date>Fri, 23 Oct 2009 04:12:00 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709348391</dc:identifier>
<dc:title><![CDATA[Do terbutaline- and mold-associated impairments of the brain and lung relate to autism?]]></dc:title>
<prism:number>9-10</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>710</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>703</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/9-10/711?rss=1">
<title><![CDATA[The treatment of patients with mycotoxin-induced disease]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/9-10/711?rss=1</link>
<description><![CDATA[<p>Twenty-eight incapacitated individuals (average 43 years old, 7 males, 21 females, range 12-70) exposed to molds and mycotoxins were studied and treated with a protocol of cleaning up or changing their environment to be mold free. Injections of the optimum dose of antigens were given as part of the treatment protocol as was oral and intravenous (i.v.) antioxidants; heat depuration (sauna); physical therapy with massage and exercise under environmentally controlled conditions; oxygen therapy at 4-8 L/min for 2 hours with a special wood-grade cellophane reservoir and a glass oxygen container. Many patients were sensitive to plastics; therefore, exposures to these were kept to a minimum. Autogenous lymphocytic factor was given as an immune modulator. Of 28 patients, 27 did well and returned to work. One patient improved but did not return to work during the period of study.</p>]]></description>
<dc:creator><![CDATA[Rea, W. J, Pan, Y., Griffiths, B.]]></dc:creator>
<dc:date>Fri, 23 Oct 2009 04:12:00 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709348281</dc:identifier>
<dc:title><![CDATA[The treatment of patients with mycotoxin-induced disease]]></dc:title>
<prism:number>9-10</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>714</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>711</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/9-10/715?rss=1">
<title><![CDATA[Molds, mycotoxins, and nutrition]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/9-10/715?rss=1</link>
<description><![CDATA[<p>Many of the patients with mold and chemical exposure that come to Environmental Health Center &mdash; Dallas (EHC-D) show signs of impaired digestion. Improving their digestion improves their nutritional status and also improves their detoxification abilities. Mold and chemical exposure also affect the patient&rsquo;s short-term memory and executive function. This presents a challenge when it comes to teaching the patient how to improve their nutritional status and detoxification. At the EHC-D, we use several instructions methods that have resulted in the patient&rsquo;s grasping the concepts and then being able to implement the required changes.</p>]]></description>
<dc:creator><![CDATA[Overberg, R.]]></dc:creator>
<dc:date>Fri, 23 Oct 2009 04:12:00 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709348278</dc:identifier>
<dc:title><![CDATA[Molds, mycotoxins, and nutrition]]></dc:title>
<prism:number>9-10</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>722</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>715</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/9-10/723?rss=1">
<title><![CDATA[Mold remediation in a hospital]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/9-10/723?rss=1</link>
<description><![CDATA[<p>As occupants in a hospital, patients are susceptible to air contaminants that can include biological agents dispersed throughout the premise. An exposed patient can become ill and require medical intervention. A consideration for patients is that they may have become environmentally sensitive and require placement in an environment that does not compromise their health. Unfortunately, the hospital environment often contains more biological substances than can be expected in an office or home environment. When a hospital also experiences water intrusion such as flooding or water leaks, resulting mold growth can seriously compromise the health of patients and others such as nursing staff and physicians (Burge, Indoor Air and Infectious Disease. Occupational Medicine: State of the Art Reviews, 1980; Lutz et al., Clinical Infectious Diseases 37: 786&mdash;793, 2003). Micro-organism growth can propagate if the water is not addressed quickly and effectively. Immunocompromised patients are particularly at risk when subjected to fungal infection such that the US Center for Disease Control issued guideline for building mold in health care facilities (Centers for Disease and Control [CDC], Centers for Disease and Control: Questions and Answers on Stachybotrys chartarum and Other Molds, 2000). This paper is based on mold remediation of one portion of a hospital unit due to water from construction activity and inadequate maintenance, resulting in mold growth. A large proportion of the hospital staff, primarily nurses in the dialysis unit, exhibited health symptoms consistent with mold exposure. Unfortunately, the hospital administrators did not consider the mold risk to be serious and refused an independent consultant retained by the nurse&rsquo;s union to examine the premise (Canadian Broadcasting Corporation [CBC], Nurses file complaints over mold at Foothills. Canadian Broadcasting Corporation, 2003). The nurse&rsquo;s union managed to have the premise examined by submitting a court order of detention and inspection and for an interlocutory injunction to allow their consultants to undertake air quality testing. Mold remediation procedures are readily available and are not to be discussed here (Silicato, http://www.nibs.org/BETEC/M6/ 13-Silicato_Mold-Remediation.pdf, 2004). However, the difficulty of determining the qualifications of consultants, contactors and project managers are discussed. It also describes the need and importance of a buffer zone between the occupied areas and the mold abatement containment area.</p>]]></description>
<dc:creator><![CDATA[Lee, T. G]]></dc:creator>
<dc:date>Fri, 23 Oct 2009 04:12:00 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709348394</dc:identifier>
<dc:title><![CDATA[Mold remediation in a hospital]]></dc:title>
<prism:number>9-10</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>730</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>723</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/9-10/731?rss=1">
<title><![CDATA[Creating healthier buildings]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/9-10/731?rss=1</link>
<description><![CDATA[<p>Some conventional building design, construction and maintenance practices create conditions that are capable of causing illness in healthy individuals or exacerbating illness in already sensitized individuals. Staying in faulty building environments may unnecessarily prolong environmental-related illness. Physician and patient awareness of such common building failures may help to diagnose environmental triggers of current illness. Architects would benefit from collaboration with environmental physicians to understand the importance of healthier building design to building occupants. Architectural education and practice is slowly incorporating better methods, often in the context of greening and sustainability. Architects are presently being advised that the needs of approximately 15% of the general population who are significantly sensitive cannot be ignored in building design. The author reviews a number of building failures and itemizes a set of relatively simple principles and design concepts that would help create new and renovated buildings that are healthier than current buildings.</p>]]></description>
<dc:creator><![CDATA[Small, B. M]]></dc:creator>
<dc:date>Fri, 23 Oct 2009 04:12:00 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709348284</dc:identifier>
<dc:title><![CDATA[Creating healthier buildings]]></dc:title>
<prism:number>9-10</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>735</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>731</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/reprint/25/9-10/737?rss=1">
<title><![CDATA[Towards healthy homes]]></title>
<link>http://tih.sagepub.com/cgi/reprint/25/9-10/737?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Kilburn, K. H.]]></dc:creator>
<dc:date>Fri, 23 Oct 2009 04:12:00 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709351442</dc:identifier>
<dc:title><![CDATA[Towards healthy homes]]></dc:title>
<prism:number>9-10</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>740</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>737</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/8/505?rss=1">
<title><![CDATA[Arsenic trioxide inhibits the growth of human lung cancer cell lines via cell cycle arrest and induction of apoptosis at both normoxia and hypoxia]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/8/505?rss=1</link>
<description><![CDATA[<p>Arsenic trioxide (As<SUB> 2</SUB>O<SUB>3</SUB>) has been established to be an effective agent for treating acute promyleocytic leukemia. Laboratory data suggest that As<SUB>2</SUB>O<SUB> 3</SUB> induces apoptosis of several solid tumor cells including lung cancer cells. Regions of tissue hypoxia often arise in aggressive solid tumors, and hypoxic tumors exhibit augmented invasiveness and metastatic ability in several malignancies. Furthermore, hypoxia may impair the treatment efficiency; therefore, we studied the cytotoxic effect of As<SUB>2</SUB>O<SUB>3</SUB> on human lung adenocarcinoma cell lines A549 and A549/R (resistant to vincristine, adriamycin and mitomycin etc.) grown under normoxic and hypoxic (1% oxygen) conditions. At both normoxia and hypoxia, 5, 10 and 15 &micro;M As<SUB>2</SUB>O<SUB>3</SUB> induced evident growth inhibition and apoptosis in A549 cells as well as A549/R cells after 48 hours of exposure. In contrast, the conventional chemotherapeutic drug vincristine showed lowered efficiency in hypoxic A549 cells. As<SUB>2</SUB>O<SUB>3</SUB> induced G<SUB>2</SUB>/M cell cycle arrest in both normoxic and hypoxic A549 cells. As<SUB>2</SUB>O<SUB>3</SUB> significantly decreased the messenger RNA (mRNA) levels of Cyclin B<SUB>1</SUB> and survivin and the protein levels of Cyclin B<SUB>1</SUB>, phospho-CDC<SUB>2</SUB> (Thr 161) and survivin in both normoxic and hypoxic A549 cells. Together, our findings indicated that As<SUB>2</SUB>O<SUB>3</SUB> significantly inhibited the proliferation of lung cancer cells via G<SUB>2</SUB>/M cell cycle arrest and induction of apoptosis at both normoxia and hypoxia, and the induction of apoptosis was associated with down regulation of survivin.</p>]]></description>
<dc:creator><![CDATA[Ge-ping, Q., Qing-Yu, X., Bing, L., Yong-an, L., Ling-Zhen, Z.]]></dc:creator>
<dc:date>Tue, 13 Oct 2009 02:33:23 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709345936</dc:identifier>
<dc:title><![CDATA[Arsenic trioxide inhibits the growth of human lung cancer cell lines via cell cycle arrest and induction of apoptosis at both normoxia and hypoxia]]></dc:title>
<prism:number>8</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>515</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>505</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/8/517?rss=1">
<title><![CDATA[Lindane residues in cultivated cucumber and in the most consumed fish in Caspian Sea (Iran)]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/8/517?rss=1</link>
<description><![CDATA[<p>In this study, the concentrations of lindane residues (organochlorine pesticides) were analyzed in samples of cultivated cucumbers (<I>Cucumis sativus L.</I>) and four species of most consumed fish (Sefid, Koli, Kilca and Kafal fish). Samples of cucumber were collected from five sites in Sari city (north, south, east, west and central areas) and samples of fish were caught using electric fishing from four major fishing centers (Chalous and Babolsar cities, Khazar Abad and Miankaleh regions) in Mazandaran province of Iran. Quantitative determination of the lindane content was performed by gas chromatography electron-capture detection (GC-ECD). The results showed that the concentration of lindane in cucumber samples and in the dorsal muscle of the selected fish were less than the Food and Agriculture Organization/World Health Organization (FAO/WHO) recommended intake.</p>]]></description>
<dc:creator><![CDATA[M, S., SS, S. S., Y, Z. Y.]]></dc:creator>
<dc:date>Tue, 13 Oct 2009 02:33:23 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709345941</dc:identifier>
<dc:title><![CDATA[Lindane residues in cultivated cucumber and in the most consumed fish in Caspian Sea (Iran)]]></dc:title>
<prism:number>8</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>523</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>517</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/8/525?rss=1">
<title><![CDATA[Metabolism of ethanol to acetaldehyde and increased susceptibility to oxidative stress could play a role in the ovarian tissue cell injury promoted by alcohol drinking]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/8/525?rss=1</link>
<description><![CDATA[<p>It is known that drinking alcohol can lead to reproductive problems in women. In this study, we analyzed the possibility that part of those effects were mediated through alterations of ovarian function related to ethanol oxidation to acetaldehyde occurring in situ. Biotransformation in the rat ovary cytosolic fraction was partially inhibited by allopurinol, suggesting the participation of xanthine oxidoreductase in the process. Microsomal pathway was of enzymatic nature, requiring nicotinamide adenine dinucleotide phosphate-oxidase (NADPH), sensitive to oxygen and significantly inhibited by sodium diethyldithiocarbamate, 4-methylpyrazole and diphenyleneiodonium. Aldehyde dehydrogenase activity was detected by histochemistry in the ovarian tissue, in the strome surrounding the follicle while no alcohol dehydrogenase was detected. However, biochemical determination of alcohol dehydrogenase and aldehyde dehydrogenase activities in rat ovarian tissue revealed the presence of some activity of both enzymes but significantly lower than those found in the liver. By repetitive exposure of animals to ethanol, the microsomal metabolism to acetaldehyde was increased but not in the case of the cytosolic fraction. In these animals, t-butylhydroperoxyde-promoted chemiluminiscence was increased in comparison to control, revealing an increased susceptibility to oxidative stress due to alcohol drinking. Ultrastructure of ovarian tissue from rats exposed chronically to alcohol revealed alterations at the level of the granulosa; theca interna and pellucida zones. In the secondary follicle, alterations consisted of marked condensation of chromatin attached to the nuclear inner membrane. Intense dilatation of the outer perinuclear space could be observed. There was a marked dilatation of the rough endoplasmic reticulum accompanied of significant detachment of ribosomes from their membranes. Mitochondria appeared swollen. In the zona pellucida, most of the cell processes from oocyte and corona radiata cells were absent or broken totally or in part. Results suggest that in the rat ovary, metabolism of ethanol to acetaldehyde may play a role in alcohol effects on female reproductive function.</p>]]></description>
<dc:creator><![CDATA[Faut, M., Rodriguez de Castro, C., Bietto, F. M, Castro, J. A, Castro, G. D]]></dc:creator>
<dc:date>Tue, 13 Oct 2009 02:33:23 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709345937</dc:identifier>
<dc:title><![CDATA[Metabolism of ethanol to acetaldehyde and increased susceptibility to oxidative stress could play a role in the ovarian tissue cell injury promoted by alcohol drinking]]></dc:title>
<prism:number>8</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>538</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>525</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/8/539?rss=1">
<title><![CDATA[Effect of resveratrol on tubular damage and interstitial fibrosis in kidneys of rats exposed to cigarette smoke]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/8/539?rss=1</link>
<description><![CDATA[<p>The aim of this study was to evaluate the effect of resveratrol on kidney tissue of rats exposed to cigarette smoke. Forty adult male Wistar Albino rats were divided into four groups. Animals in group 1 was the control group. For 6 weeks, group 2 was exposed to cigarette smoke; group 3 received daily intraperitoneal injections of resveratrol (10 mg/kg/d); and group 4 was exposed to both cigarette smoke and intraperitoneal resveratrol. All rats were sacrificed with cervical dislocation. The kidney tissues were obtained, fixed in Bouin&rsquo;s fixative and embeded in paraffin blocks. Samples were sectioned to 4-5 microns thickness, stained with hematoxylin/eosin (H/E), Masson&rsquo;s trichromic, periodic acid-schiff (PAS) and were examined by light microscopy for tubular injury and interstitial fibrosis. Results were compared by non-parametric tests. Hydropic degeneration, tubular atrophy, tubulo-interstitial fibrosis, interstitial cell infiltration, vacuolar degeneration and desquamation were prominent in group 2. In group 4, hydropic degeneration, epithelial cell vacuolization and desquamation was not observed, but occasional tubular atrophy and dilation were observed. Our study suggests that, some morphological alterations in the rat kidney, due to cigarette smoke may be prevented by resveratrol.</p>]]></description>
<dc:creator><![CDATA[Kurus, M., Ugras, M., Esrefoglu, M.]]></dc:creator>
<dc:date>Tue, 13 Oct 2009 02:33:23 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709346755</dc:identifier>
<dc:title><![CDATA[Effect of resveratrol on tubular damage and interstitial fibrosis in kidneys of rats exposed to cigarette smoke]]></dc:title>
<prism:number>8</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>544</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>539</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/8/545?rss=1">
<title><![CDATA[Effect of toluene on erythrocyte membrane stability under in vivo and in vitro conditions with assessment of oxidant/antioxidant status]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/8/545?rss=1</link>
<description><![CDATA[<p>Toluene, an organic solvent used widely in the industry, is highly lipophilic and accumulates in the cell membrane impeding transport through it. Its metabolites cause oxygen radical formation that react with unsaturated fatty acids and proteins in erythrocytes leading to lipid peroxidation and protein breakdown. In this study, we aimed to investigate the membrane stabilizing and the oxidative stress&mdash;inducing effects of toluene in human erythrocytes. Measurements of osmotic fragility, mean corpuscular volume (MCV), oxidative stress parameters and antioxidant enzyme activities were performed simultaneously both in individuals exposed to toluene professionally (in vivo) and human erythrocytes treated with toluene (in vitro). To measure osmotic fragility, erythrocytes were placed in NaCl solutions at various concentrations (0.1% [blank], 0.38%, 0.40%, 0.42%, 0.44%, 0.46%, 0.48% and 1% [stock]). Percentage of haemolysis in each solution was calculated with respect to the 100% haemolysis in the blank solution. The erythrocyte packs prepared at the day of the above-mentioned measurements were kept at &mdash;80&deg;C until the time for determination of malonyldialdehyde and protein carbonyl levels, and catalase (CAT) and glutathione peroxidase activities as indicators of oxidative stress. Toluene increased oxidative stress parameters significantly both in vivo and in vitro; it also caused a significant decrease in the activities of antioxidant enzymes. Osmotic fragility was altered only in the case of in vitro exposure. In conclusion, toluene exposure resulted in increased lipid peroxidation and protein damage both in vivo and in vitro. Although, it is natural to expect increased osmotic fragility due to oxidative properties of toluene, its membrane-stabilizing effect overcame the oxidative properties leading to decreased osmotic fragility or preventing its deterioration in vitro and in vivo toluene exposures, respectively, in the present study.</p>]]></description>
<dc:creator><![CDATA[Karabulut, I., Balkanci, Z. D., Pehlivanoglu, B., Erdem, A., Fadillioglu, E.]]></dc:creator>
<dc:date>Tue, 13 Oct 2009 02:33:23 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709346758</dc:identifier>
<dc:title><![CDATA[Effect of toluene on erythrocyte membrane stability under in vivo and in vitro conditions with assessment of oxidant/antioxidant status]]></dc:title>
<prism:number>8</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>550</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>545</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/8/551?rss=1">
<title><![CDATA[Parachlorella beyerinckii accelerates lead excretion in mice]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/8/551?rss=1</link>
<description><![CDATA[<p>The effect of <I>Parachlorella beyerinckii</I> CK-5, previously identified as Chlorella vulgaris, on gastrointestinal absorption of lead was investigated in mice. Female ICR mice aged 7 weeks were orally administered lead acetate solution at doses of 20 mg and 40 mg of lead per mouse, with or without 100 mg of <I>P. beyerinckii</I> powder (BP). The mice were bred for 24 hours. The amount of lead excreted in feces within 24 hours, and the lead levels of the blood, liver and kidney were analyzed by atomic absorption spectrometry. The percentage of total fecal excretion in mice administered BP increased by 27.7% in 20 mg lead administered mice and 17.2% in 40 mg lead administered mice in comparison to control mice, respectively. On the other hand, the lead levels of the blood, liver and kidney of BPadministered mice at 24 hours after lead administration were 48-63% lower as compared with those of control mice. The lead adsorption ability of BP and the pepsin non-digestive residue of BP (dBP) were investigated in vitro. One hundred mg of BP and dBP could adsorb 10.6 mg and 6.0 mg of lead in a 20 mg per 10 mL of lead solution, respectively. The lead absorption abilities of BP and dBP were considered to contribute to the prevention of gastrointestinal absorption of lead and the promotion of the excretion of lead. These results suggested that BP treatment might be useful in animals and humans exposed to lead.</p>]]></description>
<dc:creator><![CDATA[Uchikawa, T., Ueno, T., Hasegawa, T., Maruyama, I., Kumamoto, S., Ando, Y.]]></dc:creator>
<dc:date>Tue, 13 Oct 2009 02:33:23 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709346759</dc:identifier>
<dc:title><![CDATA[Parachlorella beyerinckii accelerates lead excretion in mice]]></dc:title>
<prism:number>8</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>556</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>551</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/8/557?rss=1">
<title><![CDATA[Effects of methomyl on lipid peroxidation and antioxidant enzymes in rat erythrocytes: In vitro studies]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/8/557?rss=1</link>
<description><![CDATA[<p>Erythrocytes are a convenient model to understand the membrane oxidative damage induced by various xenobiotic pro-oxidants. This study was designed to investigate the possibility of methomyl (Lannate<sup>&reg;</sup> 90% SP), S-methyl N-(methylcarbamoyloxy) thioacetimidate, to induce oxidative stress response in rat erythrocytes in vitro. Erythrocytes were incubated for 4 hours at 37&deg;C with different concentrations (0.0, 0.1, 0.5, 1.0, 1.5 and 2.0 mM) of methomyl. The results showed that methomyl decreased acetylcholinesterase (AChE), superoxide dismutase (SOD) and glutathione S-transferase (GST) activities and increased level of lipid peroxidation (LPO) as well as the percentage of haemolysis. The response occurred in a concentration-dependent manner. The study suggested that methomyl has the capability to induce oxidative damage as evidenced by increasing LPO and perturbations in various antioxidant enzymes.</p>]]></description>
<dc:creator><![CDATA[Mansour, S. A, Mossa, A.-T. H, Heikal, T. M]]></dc:creator>
<dc:date>Tue, 13 Oct 2009 02:33:23 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709349829</dc:identifier>
<dc:title><![CDATA[Effects of methomyl on lipid peroxidation and antioxidant enzymes in rat erythrocytes: In vitro studies]]></dc:title>
<prism:number>8</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>563</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>557</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/7/441?rss=1">
<title><![CDATA[Microbial toxin's effect on mitochondrial survival by increasing K+ uptake]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/7/441?rss=1</link>
<description><![CDATA[<p>We studied the effects of toxins, which inhibited the motility of boar spermatozoa, on rat liver mitochondria. The toxins studied were originally from bacteria isolated from moisture-damaged buildings where inhabitants exhibited symptoms, or from food causing poisoning. Some strains of Bacillus cereus and Streptomyces griseus produced potassium ionophoric peptides cereulide and valinomycin (Mikkola, et al., European Journal of Biochemistry 1999; 263: 112&mdash;117). Of interest is that channels were formed in black-lipid membranes (BLM) with a selectivity of K<sup>+</sup> &gt; Na<sup>+</sup> at a concentration of 26 nM. Recently, bafilomycin A1&mdash;an inhibitor of V-H<sup>+</sup>ATPases&mdash;was found also to be a K<sup>+</sup>-specific ionophore active at nanomolar concentrations (Teplova, et al., J Bioenerg Biomembr 2007; 39: 321&mdash;329), while B. amyloliquefaciens produced amylosin, a cation channel-forming peptide with a higher selectivity for K<sup>+</sup> over Na<sup>+</sup> at around 200 nM concentrations (Mikkola, et al., Toxicon 2007; 49: 1158&mdash;1171). Of interest is that channels were formed in BLM with a selectivity of K<sup>+</sup> &gt; Na<sup>+</sup> at a concentration of 26 nM. The ionophores and the channel-forming amylosin caused swelling of energized mitochondria due to uptake of K<sup>+</sup>, loss of membrane potential, inhibition of maximal respiration rates due to loss of pyridine nucleotides, and inhibition of ATP synthesis. Various cell types may have different sensitivities to the effects of the ionophores. Thus, the mitochondrial membrane potential in neuronal cells was more sensitive to cereulide than in differentiated Paju cells (Teplova, et al., Acta Biochimica Polonica 2004; 51: 539&mdash;544). Swelling causes release of proapoptotic factors from mitochondria, which explains that undifferentiated neuronal cells were sensitive, while differentiated Paju cells were resistant, which probably is due to them having an increased expression of the antiapoptotic protein Bcl-2 and the neuroprotective stanniocalcin.</p>]]></description>
<dc:creator><![CDATA[Saris, N-E. L., Andersson, M. A, Mikkola, R., Andersson, L. C, Teplova, V. V, Grigoriev, P. A, Salkinoja-Salonen, M. S]]></dc:creator>
<dc:date>Fri, 25 Sep 2009 02:59:05 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709103405</dc:identifier>
<dc:title><![CDATA[Microbial toxin's effect on mitochondrial survival by increasing K+ uptake]]></dc:title>
<prism:number>7</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>446</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>441</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/7/447?rss=1">
<title><![CDATA[Impairment of endothelium-dependent vasorelaxation in cadmium-hypertensive rats]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/7/447?rss=1</link>
<description><![CDATA[<p>Abnormalities in the production and/or release of relaxing factors from the endothelium have been implicated in the development of hypertension in several animal models. Endothelium-dependent relaxation has been reported to be impaired in thoracic aorta in experimentally induced and genetically hypertensive rats. Present study has extented these observations to thoracic aorta of cadmium-hypertensive rats. The possible role of alterations in oxidant status was also studied. Hypertension was induced by the intraperitoneal administration of 1 mg/kg/day cadmium for 15 days. Mechanical responses produced by acetylcholine (ACh, 10<sup>&mdash; 9</sup>&mdash;10<sup>&mdash;4</sup> M) and sodium nitroprusside (SNP, 10<sup>&mdash;10</sup>&mdash;10<sup>&mdash; 5</sup> M) were studied on phenylephrine-precontracted thoracic aorta rings from control and cadmium-hypertensive rats. Serum nitric oxide (NO) and aortic malondialdehyde (MDA) levels were measured. ACh-induced relaxation was attenuated in aorta from cadmium-hypertensive rats, whereas relaxation responses to SNP did not differ significantly between the groups. Exposure of aortic rings to N<sup>G</sup>-nitro-L-arginine methyl ester (L-NAME, 10<sup> &mdash;4</sup> M) resulted in a significantly greater inhibition of relaxation response to ACh in aortic rings of cadmium-hypertensive rats as compared with control rats. Incubation with L-arginine (L-Arg, 10<sup> &mdash;3</sup> M) caused a similar reversal of the inhibition of ACh-induced relaxation by L-NAME in both groups. Serum NO levels were decreased and aortic MDA levels were increased in cadmium-treated rats as compared with control rats. However, the differences between the groups did not reach a statistical significance. These findings suggested that the reduction in endothelium-dependent relaxation may play a role in cadmium-induced hypertension as it was in many other hypertension models.</p>]]></description>
<dc:creator><![CDATA[Gokalp, O., Ozdem, S., Donmez, S., Dogan, M., Demirin, H., Kara, Y., Sutcu, R., Cicek, E., Ozer, M., Delibas, N.]]></dc:creator>
<dc:date>Fri, 25 Sep 2009 02:59:05 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709106822</dc:identifier>
<dc:title><![CDATA[Impairment of endothelium-dependent vasorelaxation in cadmium-hypertensive rats]]></dc:title>
<prism:number>7</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>453</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>447</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/7/455?rss=1">
<title><![CDATA[Inhalation of formaldehyde and xylene induces apoptotic cell death in the lung tissue]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/7/455?rss=1</link>
<description><![CDATA[<p>The aim of this study was to determine the localization and number of apoptotic cells in lung tissue and bronchus-associated lymphoid tissue (BALT) of newborns, young, and adult rats exposed to formaldehyde (6 ppm) or technical xylene (300 ppm) for 6 weeks (8 h/day). A total of 27 female Sprague-Dawley rats were used. Apoptotic cells were mainly localized around the bronchus and bronchioles and relatively less frequently on the walls of alveoli and interalveolar septa both in control and experimental groups. In the BALT, reactive cells were localized in the area under the epithelium and distributed homogenously within the lymphoid follicles. The numbers of apoptotic cells in the lung tissue including the BALT were significantly higher in young and adult rats exposed to formaldehyde and xylene than those detected in control groups.</p>]]></description>
<dc:creator><![CDATA[Sandikci, M., Seyrek, K., Aksit, H., Kose, H.]]></dc:creator>
<dc:date>Fri, 25 Sep 2009 02:59:05 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709106824</dc:identifier>
<dc:title><![CDATA[Inhalation of formaldehyde and xylene induces apoptotic cell death in the lung tissue]]></dc:title>
<prism:number>7</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>461</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>455</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/7/463?rss=1">
<title><![CDATA[Mercury vapor inhalation and its effect on glutathione peroxidase in goldsmiths exposed occupationally]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/7/463?rss=1</link>
<description><![CDATA[<p>In the gold ornaments manufacturing cottage industries, the gold metal grain dust waste particles are recovered from mercury (Hg) amalgam. The results on air samples from these industries during the recovery process have shown a high prevalence of Hg vapor (42.7 mg/m<sup>3</sup>). The blood concentration of Hg is elevated (79.1 &micro;g/L) among workers when their blood samples are tested. The Hg toxicity is reflected in the reduction of glutathione peroxidase enzyme activity in RBC (49.317 mg/L of RBC) when compared with the data from control subjects (68.536 mg/L of RBC). These values are statistically significant. This would suggest that the Hg poisoning in goldsmiths is due to exposure. The results are discussed with relation to preventive measures.</p>]]></description>
<dc:creator><![CDATA[Jayaprakash, K.]]></dc:creator>
<dc:date>Fri, 25 Sep 2009 02:59:05 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709106769</dc:identifier>
<dc:title><![CDATA[Mercury vapor inhalation and its effect on glutathione peroxidase in goldsmiths exposed occupationally]]></dc:title>
<prism:number>7</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>465</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>463</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/7/467?rss=1">
<title><![CDATA[Evaluation of genotoxicity of pan masala employing chromosomal aberration and micronucleus assay in bone marrow cells of the mice]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/7/467?rss=1</link>
<description><![CDATA[<p>Pan masala is commonly consumed in south-east Asian and other oriental countries as an alternate of tobacco chewing and smoking. Genotoxic potential of pan masala (pan masala plain and pan masala with tobacco known as gutkha) was evaluated employing chromosome aberration (CA) and micronucleus (MN) assay in vivo. Animals were exposed to three different doses (0.5%, 1.5% and 3%) of pan masala plain (PMP) and gutkha (PMT) through feed for a period of 6 months and micronucleus and chromosomal aberrations were studied in the bone marrow cells. Induction of mean micronuclei in polychromatic erythrocytes (MNPCE) and normochromatic erythrocyte (MNNCE) was higher in both types of pan masala treated groups with respect to control group. Both pan masala plain and gutkha treatment significantly induced the frequency of MNPCE and MNNCE in the bone marrow cells, indicating the genotoxic potential. Furthermore, slight decline in the ratio of polychromatic erythrocytes to normochromatic erythrocytes was also noticed, suggesting the cytotoxic potential even though the ratio was statistically non significant. A dose-dependent, significant increase in chromosome aberration was observed in both types of pan masala treated mice with respect to control. However, no significant difference in micronucleus and chromosomal aberration induction was noticed between two types of pan masala exposed (PMP and PMT) groups. Results suggest that both types of pan masala, i.e. plain and gutkha, have genotoxic potential.</p>]]></description>
<dc:creator><![CDATA[Mojidra, B., Archana, K., Gautam, A., Verma, Y., Lakkad, B., Kumar, S.]]></dc:creator>
<dc:date>Fri, 25 Sep 2009 02:59:05 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709345939</dc:identifier>
<dc:title><![CDATA[Evaluation of genotoxicity of pan masala employing chromosomal aberration and micronucleus assay in bone marrow cells of the mice]]></dc:title>
<prism:number>7</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>471</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>467</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/7/473?rss=1">
<title><![CDATA[Transforming growth factor-{beta}3 expression up-regulates on cleft palates induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin in mice]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/7/473?rss=1</link>
<description><![CDATA[<p>2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) has been shown to induce cleft palate, in which the molecular etiology of the defect is poorly characterized. Recently, transforming growth factor-&beta;3 (TGF-&beta;3) has been indicated to play an essential role in the development of palatal shelves. In this developmental toxicity study, we investigated the effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the expression of TGF-&beta;3 in fetal mice. Pregnant C57BL/6 mice were exposed to corn oil or TCDD (32 &micro;g/kg/day 64 &micro;g/kg/day, per os) at embryonic day 10 (ED10), a drastic inhibition of palatal shelves was induced. By using RT-PCR (reverse transcription-polymerase chain reaction) and Western blot, the expressions of TGF-&beta;3 was investigated. We found that the expression of TGF-&beta;3 was gradually up-regulated in TCDD-treated group. These results suggest that cleft palate can be induced by TCDD exposure, the modification of TGF-&beta;3 is related to its pathogenesis.</p>]]></description>
<dc:creator><![CDATA[Gan, L.-q., Fu, Y.-x., Liu, X., Qiu, L., Wu, S.-d., Tian, X.-f., Liu, Y., Wei, G.-h.]]></dc:creator>
<dc:date>Fri, 25 Sep 2009 02:59:05 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709345940</dc:identifier>
<dc:title><![CDATA[Transforming growth factor-{beta}3 expression up-regulates on cleft palates induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin in mice]]></dc:title>
<prism:number>7</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>478</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>473</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/7/479?rss=1">
<title><![CDATA[The effect of the prenatal and post-natal long-term exposure to 50 Hz electric field on growth, pubertal development and IGF-1 levels in female Wistar rats]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/7/479?rss=1</link>
<description><![CDATA[<p>To investigate prenatal and post-natal effects of extremely low frequency (ELF) electric field (EF) on growth and pubertal development, pregnant Wistar rats were randomly distributed among three groups. The pregnant rats of the prenatal group were exposed to 24-hour EF at 50 Hz EF 10 kV/min during pregnancy and their subsequent randomly selected female pups continued to be exposed until puberty. The post-natal group was unexposed to EF during pregnancy, but randomly selected female pups from this group were exposed to EF between delivery and puberty at the same doses and duration as the prenatal group. The third group was a sham-exposed group. The mean birth weight and weight gain of the pups during study period were found significantly reduced in prenatal group than post-natal and sham-exposed groups (p &lt; 0.001). No difference could be found among the three groups for body weight at puberty (p &gt; 0.05). The mean age at vaginal opening and estrous were significantly higher at prenatal group than post-natal and sham-exposed groups (p &lt; 0.001). Serum insulin-like growth hormone-1 (IGF-1) levels were found significantly reduced in prenatal exposure group compared with the other two groups (p &lt; 0.001). There was no difference for birth weight, weight gain, the mean age at vaginal opening and estrous and IGF-1 levels between post-natal and sham-exposed groups (p &gt; 0.05). There was also no difference for FSH, LH and E2 levels at puberty among the three groups (p &gt; 0.05). Histological examination revealed that both the prenatal and post-natal groups had the evidence of tissue damage on hypothalamus, pituitary gland and ovaries. In conclusion, early beginning of prenatal exposure of rats to 24 hours 50 Hz EF at 10 kV/m until puberty without magnetic field (MF) resulted in growth restriction, delayed puberty and reduced IGF-1 levels in female Wistar rats. These effects probably associated with direct toxic effects of EF on target organs. Post-natal exposure to EF at similar doses and duration seems to be less harmful on target organs. Post-natal exposure to EF at similar doses and duration seems to be less harmful.</p>]]></description>
<dc:creator><![CDATA[Dundar, B., Cesur, G., Comlekci, S., Songur, A., Gokcimen, A., Sahin, O., Ulukut, O., Yilmaz, H. R., Sutcu, R., Caliskan, S.]]></dc:creator>
<dc:date>Fri, 25 Sep 2009 02:59:05 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709345942</dc:identifier>
<dc:title><![CDATA[The effect of the prenatal and post-natal long-term exposure to 50 Hz electric field on growth, pubertal development and IGF-1 levels in female Wistar rats]]></dc:title>
<prism:number>7</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>487</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>479</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/7/489?rss=1">
<title><![CDATA[Effects of piperonyl butoxide on spontaneous behavior in F1-generation mice]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/7/489?rss=1</link>
<description><![CDATA[<p>Piperonyl butoxide was given in the diet to provide levels of 0 (control), 0.02%, 0.06%, and 0.18% from 5 weeks of age of the F<SUB>0</SUB> generation to 12 weeks of age of the F<SUB>1</SUB> generation in mice. Select reproductive and neurobehavioral parameters were then measured. In exploratory behavior in the F<SUB>0</SUB> generation, vertical time of adult females increased significantly in a dose-related manner. In behavioral developmental parameters, cliff avoidance was delayed significantly in the high-dose group in male offspring, and this effect was significantly dose-related. In female offspring, surface righting was significantly delayed in the high-dose group, and this effect was significantly dose-related. In spontaneous behavior in the F<SUB>1</SUB> generation, females showed more activities in some variables in the high-dose group. Dose levels of piperonyl butoxide used in the present study produced several adverse effects in neurobehavioral parameters in mice.</p>]]></description>
<dc:creator><![CDATA[Tanaka, T., Takahashi, O., Oishi, S., Ogata, A.]]></dc:creator>
<dc:date>Fri, 25 Sep 2009 02:59:05 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709346756</dc:identifier>
<dc:title><![CDATA[Effects of piperonyl butoxide on spontaneous behavior in F1-generation mice]]></dc:title>
<prism:number>7</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>497</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>489</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/6/377?rss=1">
<title><![CDATA[Chronic prenatal exposure to the 900 megahertz electromagnetic field induces pyramidal cell loss in the hippocampus of newborn rats]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/6/377?rss=1</link>
<description><![CDATA[<p>Widespread use of mobile phones which are a major source of electromagnetic fields might affect living organisms. However, there has been no investigation concerning prenatal exposure to electromagnetic fields or their roles in the development of the pyramidal cells of the cornu ammonis in postnatal life. Two groups of pregnant rats, a control group and an experimental group, that were exposed to an electromagnetic field were used. For obtaining electromagnetic field offspring, the pregnant rats were exposed to 900 megahertz electromagnetic fields during the 1&ndash;19th gestation days. There were no actions performed on the control group during the same period. The offspring rats were spontaneously delivered&mdash;control group (<I>n</I>&nbsp;=&nbsp;6) and electromagnetic field group (<I>n</I>&nbsp;=&nbsp;6). Offspring were sacrificed for stereological analyses at the end of the 4th week. Pyramidal cell number in rat cornu ammonis was estimated using the optical fractionator technique. It was found that 900 megahertz of electromagnetic field significantly reduced the total pyramidal cell number in the cornu ammonis of the electromagnetic field group (<I>P</I>&nbsp;&lt;&nbsp;0.001). Therefore, although its exact mechanism is not clear, it is suggested that pyramidal cell loss in the cornu ammonis could be due to the 900 megahertz electromagnetic field exposure in the prenatal period.</p>]]></description>
<dc:creator><![CDATA[Bas, O, Odaci, E, Mollaoglu, H, Ucok, K, Kaplan, S]]></dc:creator>
<dc:date>Tue, 11 Aug 2009 06:32:05 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709106442</dc:identifier>
<dc:title><![CDATA[Chronic prenatal exposure to the 900 megahertz electromagnetic field induces pyramidal cell loss in the hippocampus of newborn rats]]></dc:title>
<prism:number>6</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>384</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>377</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/6/385?rss=1">
<title><![CDATA[Effect of melatonin and vitamin C on expression of endothelial NOS in heart of chronic alcoholic rats]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/6/385?rss=1</link>
<description><![CDATA[<p>The aim of this study was to investigate the effects of melatonin and vitamin C on expression of endothelial nitric oxide synthase (NOS) in heart tissue of chronic alcoholic rats. Twenty-four adult male Wistar rats weighing 200&ndash;250&nbsp;g were used in this study. Rats were divided into four groups. The first group served as control (<I>n</I>&nbsp;=&nbsp;6). The second group was treated with ethanol (%7.2) for 28&nbsp;days (<I>n</I>&nbsp;=&nbsp;6), which was administered in artificial isocaloric diets. The third group was given ethanol and supplemented with 40&nbsp;mg/kg vitamin C [intraperitoneally (i.p.)] (<I>n</I>&nbsp;=&nbsp;6). The fourth group was given ethanol and supplemented with 4&nbsp;mg/kg melatonin (i.p.) (<I>n</I>&nbsp;=&nbsp;6). At the end of the experiment, rats were sacrificed and heart tissues were processed for immunohistochemistry analysis to endothelial NOS (eNOS). eNOS immunoreactivity showed heterogeneous distribution in control group. eNOS immunoreactivity was (+) in some myocytes and (++) in some others. Expression of eNOS in alcohol group was heterogeneous like control group but also stronger than that. Immunoreactivity was (+++) in myocytes near the epicardial zone and (++) in myocytes near the endocardium border. In melatonin and vitamin C-treated groups, eNOS immunoreactivity was diffuse and the intensity of reaction was (+++) in subepicardial region. However, eNOS immunoreactivity scores were weaker in these groups when compared with the alcohol group. Our results indicate that alleviation of oxidative stress by antioxidant therapy reduces reactive oxygen species-mediated nitric oxide inactivation.</p>]]></description>
<dc:creator><![CDATA[Sonmez, M., Narin, F, Akkus, D, Ozdamar, S]]></dc:creator>
<dc:date>Tue, 11 Aug 2009 06:32:05 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709106444</dc:identifier>
<dc:title><![CDATA[Effect of melatonin and vitamin C on expression of endothelial NOS in heart of chronic alcoholic rats]]></dc:title>
<prism:number>6</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>393</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>385</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/6/395?rss=1">
<title><![CDATA[Follicle-stimulating hormone levels in male workers exposed to urban chemical, physical, and psychosocial stressors]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/6/395?rss=1</link>
<description><![CDATA[<p>The aim of this study is to evaluate whether occupational exposure to urban stressors could cause alterations in the follicle-stimulating hormone (FSH) levels in traffic policemen compared to a control group. After excluding the subjects with main confounding factors, traffic policemen and male controls were matched by age, working life, body mass index (BMI), drinking habit, cigarette smoking history, and daily consumption of Italian coffee, 166 traffic policemen and 166 controls were included into the study. FSH levels were significantly higher in traffic policemen compared to male controls (<I>P</I>&nbsp;&lt;&nbsp;0.05). The distribution of FSH values in traffic policemen and controls was significant (<I>P</I>&nbsp;&lt;&nbsp;0.05). Our results suggest that occupational exposure to low doses of chemical and psychosocial stressors may alter plasma levels of FSH in traffic policemen more than in the control group. If the results obtained are confirmed by further research, the plasma levels of FSH may be used as early biological markers, valuable for the group, used in occupational set even before the appearance of disorders of male fertility.</p>]]></description>
<dc:creator><![CDATA[Tomei, G, Tomao, E, Ciarrocca, M, Rosati, M., Caciari, T, Gamberale, D, Palermo, P, Sio, S D., Tria, M, Panfili, A, Tomei, F]]></dc:creator>
<dc:date>Tue, 11 Aug 2009 06:32:05 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709106466</dc:identifier>
<dc:title><![CDATA[Follicle-stimulating hormone levels in male workers exposed to urban chemical, physical, and psychosocial stressors]]></dc:title>
<prism:number>6</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>402</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>395</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/6/403?rss=1">
<title><![CDATA[Phylogenetic analysis of ALAD and MGP genes related to lead toxicity]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/6/403?rss=1</link>
<description><![CDATA[<p>Experimental studies in our laboratory have established the role of -aminolevulinic acid dehydratase (ALAD) and matrix -carboxyglutamic acid (MGP) gene polymorphisms in the etiology of lead toxicity. Polymorphisms in these genes influenced the levels of lead in subjects exposed to this metal. In extension to our studies, we aimed to investigate the possible role of these proteins in evolution by studying the phylogenetic relationship and divergence of ALAD and MGP genes using computational phylogenetic methods. The human ALAD and MGP protein sequences from various species were retrieved from Swiss-Prot database and were compared using Basic Local Alignment Search Tool. Multiple sequence alignment was carried out using ClustalW with defaults, and phylogenetic trees for both the genes were built using neighbor-joining method as in Mega software. Our study indicated that ALAD is a highly conserved protein with the same metal binding site distributed in all the phyla (from archaea to chordates). Phylogenetic analysis of MGP gene revealed that it had an important role in the evolution of endogenous skeleton in contrast to exoskeleton of insects. Occurrence of these genes in evolution with conserved metal binding sites strengthens the role of ALAD and MGP genes in regulating heme biosynthesis and mineralization, respectively, in evolution and helps in better understanding of lead poisoning.</p>]]></description>
<dc:creator><![CDATA[Shaik, A., Khan, M, Jamil, K]]></dc:creator>
<dc:date>Tue, 11 Aug 2009 06:32:05 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709106596</dc:identifier>
<dc:title><![CDATA[Phylogenetic analysis of ALAD and MGP genes related to lead toxicity]]></dc:title>
<prism:number>6</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>409</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>403</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/6/411?rss=1">
<title><![CDATA[Melatonin levels and enzymatic antioxidant defense system decrease in blood of patients with bronchial asthma]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/6/411?rss=1</link>
<description><![CDATA[<p>The etiology of bronchial asthma (BA) is not clearly understood. In recent years, a few studies have investigated the possible role of reactive oxygen species (ROS) in the etiology of BA. There are some defense mechanisms in the organism to avoid the harmful effects of ROS. Melatonin (MEL) is synthesized by the pineal gland at night and exhibits antioxidant properties. The aim of this study was to investigate serum MEL levels, erythrocyte antioxidant enzyme activities, namely superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and the association of the respiratory function tests, namely dynamic lung volumes; the forced vital capacity (FVC/L, FVC%), the forced expiratory volume in 1&nbsp;s (FEV<SUB>1</SUB>/L, FEV<SUB>1</SUB>%), and peak expiratory flow (PEF/L/s, PEF%) in 30 patients with BA and 30 age-matched healthy controls. The levels of serum MEL, the activities of erythrocyte SOD, and the values of FVC/L, FVC%, FEV<SUB>1</SUB>/L, and FEV<SUB>1</SUB>% were significantly lower in the patients with BA than in control group. The positive correlations were observed between FVC% with erythrocyte SOD and GSH-Px, FEV<SUB>1</SUB>/L as well as FEV<SUB>1</SUB>% with erythrocyte SOD, whereas negative correlation was observed between PEF/L/s with levels of serum MEL. In conclusion, these results provide some evidence for a potential role of decreased antioxidant enzymes, MEL, and respiratory function test values in BA.</p>]]></description>
<dc:creator><![CDATA[Gumral, N, Caliskan, S, Ozguner, F, Kaleli, S, Akkaya, A, Yilmaz, H, Sen, S]]></dc:creator>
<dc:date>Tue, 11 Aug 2009 06:32:05 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709106625</dc:identifier>
<dc:title><![CDATA[Melatonin levels and enzymatic antioxidant defense system decrease in blood of patients with bronchial asthma]]></dc:title>
<prism:number>6</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>416</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>411</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/6/417?rss=1">
<title><![CDATA[Hesperidin attenuates benzo[{alpha}] pyrene-induced testicular toxicity in rats via regulation of oxidant/antioxidant balance]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/6/417?rss=1</link>
<description><![CDATA[<p>Benzo[]pyrene (BaP) is one of the polycyclic aromatic hydrocarbons, which has shown carcinogenic, teratogenic, and mutagenic potentials. The reproductive toxicity of BaP in male was not well investigated. Thereby, we have addressed in the current study the testicular toxicity of BaP and the postulate whether or not the citrus flavonoid, hesperidin (HDN), could ameliorate such toxicity in male Swiss albino rats. In this sense, animals were challenged with BaP (50&nbsp;mg/kg/day, orally) for 10 consecutive days. HDN (200&nbsp;mg/kg/day, orally) was administered ahead of BaP challenge for 10 consecutive days. BaP induced testicular toxicity that was well characterized histologically and biochemically. It decreased the relative testis weight and induced pyknosis and necrobiotic changes as well as chromatolysis in the nuclei of the spermatocytes in the seminiferous tubules. It also markedly deteriorated epididymal function as shown by decreased sperm count, motility, and daily sperm production. The polyaromatic hydrocarbon also reduced the testicular activities of lactate dehydrogenase (LDH-X), superoxide dismutase (SOD), and glutathione-S-transferase (GST). Besides, it decreased the testicular reduced glutathione (GSH) but increased malondialdehyde (MDA) contents. Prior administration of HDN ahead of BaP challenge ameliorated all the histological and biochemical alterations induced by BaP. It improved the epididymal function and mitigated the injurious effects of BaP on the seminiferous tubules. In conclusion, HDN has proven protective effects in BaP-induced testicular toxicity paradigm, and this protection resides, at least in part, on its antioxidant properties.</p>]]></description>
<dc:creator><![CDATA[Arafa, H., Aly, H., Abd-Ellah, M., El-Refaey, H.]]></dc:creator>
<dc:date>Tue, 11 Aug 2009 06:32:05 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709106624</dc:identifier>
<dc:title><![CDATA[Hesperidin attenuates benzo[{alpha}] pyrene-induced testicular toxicity in rats via regulation of oxidant/antioxidant balance]]></dc:title>
<prism:number>6</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>427</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>417</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://tih.sagepub.com/cgi/content/abstract/25/6/429?rss=1">
<title><![CDATA[The protective effect of caffeic acid phenethyl ester (CAPE) on oxidative stress in rat liver exposed to the 900 MHz electromagnetic field]]></title>
<link>http://tih.sagepub.com/cgi/content/abstract/25/6/429?rss=1</link>
<description><![CDATA[<p>In this study, we aimed to investigate the possible protective effects of caffeic acid phenethyl ester (CAPE) on lipid peroxidation (LPO) and the activities of antioxidant enzymes in the liver of rats exposed to the 900&nbsp;MHz electromagnetic field (EMF). EMF of cellular phones may affect biological systems by increasing free radical, which appear mainly to enhance LPO, and by changing the antioxidative activities of liver, thus leading to oxidative damage. CAPE, an active component of propolis extract, exhibits antioxidant properties and several studies suggest that supplementation with antioxidant can influence EMF exposure induced hepatotoxicity. Thirty male Sprague-Dawley rats were divided into three groups: control (<I>n</I>&nbsp;=&nbsp;10), 900&nbsp;MHz EMF (<I>n</I>&nbsp;=&nbsp;10) and 900&nbsp;MHz EMF&nbsp;+&nbsp;CAPE (<I>n</I>&nbsp;=&nbsp;10). CAPE was injected intraperitoneally for 30&nbsp;days before exposure to EMF. Liver tissue was removed to study the activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), xanthine oxidase (XO) and the levels of LPO. The activities of XO, CAT and level of LPO increased in the 900&nbsp;MHz electromagnetic field (EMF) group compared with the control group, although XO, CAT activities and LPO levels were decreased by 900&nbsp;MHz EMF&nbsp;+&nbsp;CAPE administration. The activities of SOD and GSH-Px decreased in the 900&nbsp;MHz EMF group compared with the control group, although their levels were increased by EMF&nbsp;+&nbsp;CAPE administration. It can be concluded that CAPE may prevent the 900&nbsp;MHz EMF-induced oxidative changes in liver by strengthening the antioxidant defense system by reducing reactive oxygen species and increasing antioxidant enzyme activities.</p>]]></description>
<dc:creator><![CDATA[Koyu, A, Ozguner, F, Yilmaz, H., Uz, E, Cesur, G, Ozcelik, N]]></dc:creator>
<dc:date>Tue, 11 Aug 2009 06:32:05 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0748233709106821</dc:identifier>
<dc:title><![CDATA[The protective effect of caffeic acid phenethyl ester (CAPE) on oxidative stress in rat liver exposed to the 900 MHz electromagnetic field]]></dc:title>
<prism:number>6</prism:number>
<prism:volume>25</prism:volume>
<prism:endingPage>434</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>429</prism:startingPage>
<prism:section>Article</prism:section>
</item>

</rdf:RDF>