Renal transport of glycine during glutathione replenishment in rats

Renal transport of glycine was studied in control and glutathione-depleted rats. Diethylmaleate (4.0 mmol/kg body wt, ip) was used as a glutathione depletor agent and the studies were carried out 6 and 10 h post-diethylmaleate injection. Renal transport was measured in isolated rat kidney preparations by means of clearance techniques and in brush border membrane vesicles by a rapid filtration method. Tubular reabsorption of glycine, when compared to glomerular filtration rate, measured at different substrate tubular loads, was higher in treated kidneys. Tissue 14C accumulation was also higher in kidneys from diethylmaleate-treated animals. Studies with brush border membrane vesicles indicated that glutathione depletion induced higher sodium-dependent glycine uptake in contrast with control preparations. This adaptation was not associated with an increment in either tau-glutamyltransferase activity or in protein concentrations. These results could explain in part the replenishment of GSH cellular levels in glutathione-depleted kidneys by means of higher transport capacity for glycine (a glutathione precursor) which was maintained even when GSH levels were restored.