Hiperglicemia Y Vitamina C

Hyperglycemia inhibits the uptake of dehydroascorbate in tubular epithelial cell.
Chen L, Jia RH, Qiu CJ, Ding G.
Source
Division of Nephrology, Renmin Hospital of Wuhan University, 238 JiefangRoad, Wuhan 430060, China.
Abstract
BACKGROUND/AIMS:
Oxidative stress has been considered to be a common pathogenetic factor of diabetic nephropathy. But the reason why renal cells are susceptible tooxidative injury in diabetes is not clear. Vitamin C plays a central role in the antioxidant defense system and exists in two major forms. The charged form, ascorbate, is taken up into cells viasodium-dependent facilitated transport. The uncharged form, dehydroascorbate, enters cells via glucose transporter and is then converted back to ascorbate within these cells. Because dehydroascorbate andglucose compete for glucose transporters, hyperglycemia will exclude vitamin C from the cell and resulted in a decreased antioxidant capacity in some cell type that is dehydroascorbate dependent. Assuch, we hypothesized that some renal cells were dehydroascorbate dependent and the susceptibility of renal cells to glucose-induced injury was mediated by hyperglycemic exclusion of dehydroascorbateuptake through competing for glucose transporter. The aims of the present study were to determine whether tubular epithelial cell was dehydroascorbate dependent and the effect of dehydroascorbate onthe production of reactive oxygen species in cells incubated by high glucose.
METHODS:
Tubular epithelial cell was cultured in RPMI-1640 medium containing 10% newborn calf serum. Intracellularascorbate and dehydroascorbate contents were measured with vitamin C assay system. The intracellular formation of reactive oxygen species was detected with the fluorescent probe CM-H(2)DCFDA by usingconfocal microscopy.
RESULTS:
Ascorbate entry into the cells was not significantly different from background noise. In contrast, we observed a significant increase in the uptake of dehydroascorbate in...