High glucose-induced membrane lipid peroxidation on intact erythrocytes and on isolated erythrocyte membrane (ghosts)

Abstract

Glucose autoxidation has been proposed to play a role in diabetes complications via free radicals damage to cells, but the mechanisms that should link high glucose to oxidative stress is still partially unknown. In this study we report that high glucose induces lipid peroxidation, membrane tocopherol consumption, and lysis in intact erythrocytes (RBC), whereas antioxidant enzyme activity was not affected. On the contrary, no lipid peroxidation or free thiols oxidation was detectable in isolated erythrocyte membranes (ghosts) incubated either with glucose or methyl-glyoxal, a carbonyl molecule, non-enzymatic byproduct of high glucose metabolism. Our study indicates that the presence of transition metals is the necessary condition to induce glucose-driven lipid peroxiation and thiols oxidation. This study also suggests that the incubation of RBC with glucose concentration similar to non-controlled hyperglycaemia may led to the release of iron in redox active form.