Pyridoxine and pyridoxamine inhibits superoxide radicals and prevents lipid peroxidation, protein glycosylation, and (Na++K+)-ATPase activity reduction in high glucose-treated human erythrocytes

Vitamin B-6 (pyridoxine) supplementation has been found beneficial in preve nting diabetic neuropathy and retinopathy, and the glycosylation of protein s. Oxygen radicals and oxidative damage have been implicated in the cellula r dysfunction and complications of diabetes. This study was undertaken to t est the hypothesis that pyridoxine (P) and pyridoxamine (PM) inhibit supero xide radical production, reduce lipid peroxidation and glycosylation, and i ncrease the (Na+ + K+)-ATPase activity in high glucose-exposed red blood ce lls (RBC). Superoxide radical production was assessed by the reduction of c ytochrome C by glucose in the presence and absence of P or PM in a cell-fre e buffered solution. To examine cellular effects, washed normal human RBC w ere treated with control and high glucose concentrations with and without P or PM. Both P and PM significantly lowered lipid peroxidation and glycated hemoglobin (HbA(1)) formation in high glucose-exposed RBC. P and PM signif icantly prevented the reduction in (Na+ + K+)- ATPase activity in high gluc ose-treated RBC, Thus, P or PM can inhibit oxygen radical production, which in turn prevents the lipid peroxidation, protein glycosylation, and (Na+ K+)-ATPase activity reduction induced by the hyperglycemia. This study des cribes a new biochemical mechanism by which P or PM supplementation may del ay or inhibit the development of complications in diabetes. (C) 2001 Elsevi er Science Inc.