The in vitro effects of captopril on the levels of lipid peroxidation and glutathione of erythrocytes in type II diabetes.

Increase in lipid peroxidation (LP) is an indirect marker of free radical activation. The products of LP (malonyldialdehyde: MDA) are increased in diabetic patients, particularly those with angiopathy. Free radicals are eliminated by cellular enzymes such as superoxide dismutase, catalase and glutathione peroxidase. In this study, the effect and the mechanism of action of captopril, and angiotensin converting enzyme (ACE) inhibitor, on lipid peroxidation in erythrocytes from diabetics was investigated. LP and glutathione were studied in 10 type II diabetics (mean age: 57 +/- 10 yr, duration of diabetes: 12 +/- 6 yr) and in 10 healthy subjects (mean age: 30 +/- 5 yr). Lipid peroxidation levels were 20.69 +/- 4.68 MDA% in diabetics and 9.62 +/- 1.87 MDA% in normal subjects. The LP in erythrocytes of type II diabetics was decreased by the increasing concentrations of captopril (before captopril: 20.69 +/- 4.68, after captopril: (2 x 10(-5) M) 16.68 +/- 7.49 MDA%; (4 x 10(-5) M) 14.17 +/- 7.65 MDA%; (6 x 10(-5) M) 12.33 +/- 2.8 MDA%). No difference was found in the inhibition of LP between the captopril concentrations of 6 x 10(-5) M and 10 x 10(-5) M. After preincubation with captopril, the glutathione level did not change significantly in the diabetic and normal erythrocytes. Preincubation with 2-6 x 10(-5) M captopril showed no effect in the normal group (p > 0.05) but 10 x 10(-5) M captopril reduced lipid peroxidation (p < 0.01). In our study, the high levels of lipid peroxidation in erythrocytes from diabetic patients were decreased after preincubation with captopril. Decrease in the level of lipid peroxidation in vitro was independent of the glutathione level. Crosslink binding between MDA and captopril is suggested.