The effect of modest vitamin E supplementation on lipid peroxidation products and other cardiovascular risk factors in diabetic patients.

Among many factors, elevated lipids and lipid peroxide levels in blood are major risk factors in the development of cardiovascular disease in diabetic patients. This study has examined whether oral supplementation of vitamin E, an antioxidant, has any effect on blood lipid peroxidation products (LP) and lipid profile of diabetic patients. Thirty-five diabetics(D) were supplemented with DL-alpha-tocopherol (E) capsule (orally, 100 IU/d) or placebo (P) for three months in double-blind clinical trials. Plasma E was analyzed by HPLC and LP by the thiobarbituric acid-reactivity; serum lipids by auto-analyzer. Data were analyzed using paired t-test and Wilcoxon Signed Rank Test. Vitamin E supplementation significantly lowered LP and lipid levels in diabetic patients; there were no differences in these parameters after P supplementation. There were no differences in the duration of diabetes and ages of D between P- and E- supplemented groups. This study suggests that vitamin E supplementation significantly lowers blood LP and lipid levels in diabetic patients.

The accumulation of malonyldialdehyde, an end product of membrane lipid peroxidation, can cause potassium leak in normal and sickle red blood cells.

This study has examined the effect of malonyldialdehyde (MDA), an end product of lipid peroxidation, on the K+ leak in normal (AA) and sickle (SS) red blood cells (RBCs). In vitro MDA accumulation in human RBCs was accomplished by treating them with exogenous standard MDA. MDA accumulation assessed by the thiobarbituric acid reactivity of in vitro MDA-treated RBCs was comparable to the RBCs in hemolytic anemias. There was a significant K+ leak in AA RBCs after in vitro treatment with MDA. The effect of MDA on the K+ leak was greater in SS RBCs. The increase in cellular K+ leak was significantly positively correlated with the extent of MDA accumulation as assessed by thiobarbituric acid reactivity.