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Microbial toxin’s effect on mitochondrial survival by increasing K+ uptake

Department of Applied Chemistry and Microbiology, Viikki Biocenter, University of Helsinki, Finland, nils.saris{at}helsinki.fi; saris{at}mappi.helsinki.fi

Maria A Andersson

Department of Applied Chemistry and Microbiology, Viikki Biocenter, University of Helsinki, Finland

Raimo Mikkola

Department of Applied Chemistry and Microbiology, Viikki Biocenter, University of Helsinki, Finland

Leif C Andersson

Department of Pathology, Haartman Institute, University of Helsinki, Finland

Vera V Teplova

Institute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Pushchino, Moscow Region, Russia

Pavel A Grigoriev

Institute of Cell Biophysics, Russian Academy of Sciences, Pushchino, Moscow Region, Russia

Mirja S Salkinoja-Salonen

Department of Applied Chemistry and Microbiology, Viikki Biocenter, University of Helsinki, Finland

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—117). Of interest is that channels were formed in black-lipid membranes (BLM) with a selectivity of K⁺ > Na⁺ at a concentration of 26 nM. Recently, bafilomycin A1—an inhibitor of V-H⁺ATPases—was found also to be a K⁺-specific ionophore active at nanomolar concentrations (Teplova, et al., J Bioenerg Biomembr 2007; 39: 321—329), while B. amyloliquefaciens produced amylosin, a cation channel-forming peptide with a higher selectivity for K⁺ over Na⁺ at around 200 nM concentrations (Mikkola, et al., Toxicon 2007; 49: 1158—1171). Of interest is that channels were formed in BLM with a selectivity of K⁺ > Na⁺ at a concentration of 26 nM. The ionophores and the channel-forming amylosin caused swelling of energized mitochondria due to uptake of K⁺, 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—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.

Key Words: apoptosis • channels • ionophores • microbial • mitochondria • potassium • toxins

This version was published on August 1, 2009

Toxicology and Industrial Health, Vol. 25, No. 7, 441-446 (2009)
DOI: 10.1177/0748233709103405


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