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Mitochondrial glutathione (GSH) transport in diabetic nephropathy

Nephropathy is a serious complication of diabetes, and is associated with oxidative stress and altered mitochondrial function. We previously defined the function of the 2‐oxoglutarate (OGC; Slc25a11) and dicarboxylate (DIC; Slc25a10) carrier in the transport of GSH into renal mitochondria. Using a diabetic rat model (ip injection of streptozotocin (STZ) into male Sprague‐Dawley rats), we tested the hypothesis that diabetic nephropathy is characterized by mitochondrial dysfunction and decreased rates of GSH transport. We characterized mitochondrial function and GSH and dicarboxylate transport in isolated mitochondria from normal and STZ‐induced diabetic rats one month post‐injection (i.e., before the onset of nephropathy). Even at this early stage of diabetes, rates of succinate‐linked State 3 respiration, respiratory control ratios, activities of GSH‐dependent and other mitochondrial enzymes, and intramitochondrial concentrations of GSH were significantly higher in mitochondria from diabetic rats as compared to those from control rats. In contrast, kinetics of GSH and dicarboxylate transport were only slightly altered by diabetes. Mitochondria from diabetic rats, however, were markedly more susceptible than those from normal rats to oxidative injury.