Vitamin E effects on oxidative damage and cell morphology in AGE‐treated SH‐SY5Y cells

Abstract

Chronic hyperglycemia generates reactive oxygen species in part through the formation and downstream signaling effects of advanced glycation end products (AGEs). In cultured cells, AGEs promote apoptosis and oxidative damage and these effects are diminished by several antioxidants, including vitamin E. This work further investigated the role of vitamin E in cellular protection against AGE‐induced oxidative damage and cell morphology changes in SH‐SY5Y cells. Glycated BSA (1 mg/ml) decreased cell viability and increased lipid and protein oxidation markers in comparison to cells treated with unglycated BSA. Cotreatment with either α‐tocopherol (200 uM) or n‐acetyl‐cysteine (NAC) (2 mM) improved cell viability, but differentially affected lipid and protein oxidation markers. Although α‐tocopherol decreased lipid and protein oxidation, it had no effect on the AGE‐mediated changes in cell morphology or intracellular GSH concentration. In contrast, NAC increased cellular GSH concentrations, decreased protein oxidation, and prevented AGE‐mediated changes in cell morphology but did not affect elevated lipid oxidation. Thus, although vitamin E protects SH‐SY5Y cells against AGE‐induced macromolecular damage and improves viability, it failed to protect against cell morphology changes caused by AGEs.