| Sign In to gain access to subscriptions and/or personal tools. |
Lipoperoxidation and antioxidant capacity in patients with poorly controlled type 2 diabetesDepartment of Pharmacology, University of Florence, Florence, Italy maura.lodovici{at}unifi.it
Department of Pharmacology, University of Florence, Florence, Italy
Department of Clinical Physiopathology, Unit of Endocrinology, University of Florence, Florence, Italy
Department of Clinical Physiopathology, Unit of Endocrinology, University of Florence, Florence, Italy Type 2 diabetes is a heterogeneous disease resulting from insulin resistance and/or from a β-cell secretory defect. Hyperglycemia, which occurs during type 2 diabetes, causes disorders of oxidative–antioxidative balance in the cells, leading to increased free-radical formation. Reduced antioxidant capacity is supposed to be one of the causes of the occurrence of complications in type 2 diabetes. The aim of this study was to evaluate lipoperoxidation and plasma antioxidant status in patients with poorly controlled type 2 diabetes with or without complications. In this study, 15 patients with type 2 diabetes without complications and 11 patients with type 2 diabetes with complications were enrolled. The ferric-reducing ability of plasma showed no differences between the two experimental groups. A small, nonsignificant, Superoxide dismutase (SOD) activity reduction was observed in patients with diabetes with complications when compared to those patients with diabetes without complications; on the contrary, we found increased lipoperoxidation in patients with diabetes with complications compared with those patients with diabetes without complications. We also observed a positive correlation between malondialdehyde levels and high density lipoprotein or vitamin E in all analyzed patients with type 2 diabetes. Data obtained from our study show that patients with poorly controlled type 2 diabetes with complications have higher lipoperoxidation than patients with complication-free diabetes, although a residual compensatory response to hyperglycemia-induced oxidative stress occurs.
Key Words: diabetes HDL lipoperoxidation malondialdehyde SOD activity vitamin E
Toxicology and Industrial Health, Vol. 25, No. 4-5,
337-341 (2009) |
||||