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Lipids, apolipoproteins and lipid peroxide were measured in the sera of 29 children with insulin-dependent diabetes mellitus. Ten non-diabetic children served as controls. High-density lipoprotein (HDL) was separated by heparin-MnCl2 precipitation. Lipid peroxides in HDL and non-HDL fractions were estimated by fluorimetric measurement of thiobarbituric acid-reactive substances. The patients were normolipidemic, and their HDL-cholesterol was increased. Apo A1 level in the patients was similar to that in the controls, while levels of apo A2 and apo B were decreased in the patients. Concentrations of lipid peroxides in the whole serum and non-HDL were unaltered, while that in the HDL was higher in the patients than in the controls. Hemoglobin AIc in the patients correlated with the triglyceride and urinary excretion rate of N-acetylglucosaminidase (NAG). The NAG correlated with the triglycerides. The triglycerides correlated with the atherogenic index, apo B and total cholesterol. The lipid peroxides in the non HDL correlated with the triglyceride, atherogenic index, and NAG. That in the HDL correlated with the HDL-cholesterol, apo A1 and endogenous creatinine clearance, and inversely with the atherogenic index and apo B. Lipid peroxides in HDL and non-HDL appeared to play different physiological roles from each other, and they have provided evidence suggesting that diabetic microvascular injury is mediated by reactive oxygen species.

To determine whether oxidant-antioxidant balance is altered in chronic renal failure, antioxidant enzymes and lipid peroxide in peripheral blood cells and lipid peroxide in plasma were measured. Nine children and adolescents maintained on hemodialysis (HD), 9 on continuous ambulatory peritoneal dialysis (CAPD), and 14 controls were studied. Lipid peroxide was assayed fluorimetrically as thiobarbituric acid-reactive substance, superoxide dismutases by radioimmunoassays. Both manganese and copper-zinc superoxide dismutases in lymphocytes and monocytes in the HD and CAPD patients, and manganese superoxide dismutase in polymorphs in the HD patients were higher than in the controls. Copper-zinc superoxide dismutase, glutathione peroxidase, and catalase in erythrocytes were unaltered. The lipid peroxide level in plasma in the dialyzed patients was increased, whereas those in polymorphs and lymphocytes were unaltered. Triglyceride and total cholesterol in plasma in the dialyzed patients were also increased. The plasma lipid peroxide in the patients correlated with the triglyceride and total cholesterol level. This is the first study in which manganese superoxide dismutase is measured in nucleated cells of the patients with chronic renal failure. The present results suggest that increased superoxide dismutases protect against oxidative stress induced by chronic renal failure in nucleated cells but in either erythrocytes nor plasma.