EFFECT OF PYRIDOXINE ON SODIUM GLYCOLATE-INDUCED HYPEROXALURIA IN RATS

Large doses of pyridoxine administration (10 mg pyridoxine-HCl/100 g BW[body wt]/day) failed to lower the hyperoxaluria in rats induced by sodium glycolate feeding (100 mg/100 g BW/day). Urinary excretion of Ca was significantly decreased (P < 0.01) after the 1st wk of glycolate treatment in both pyridoxine supplemented and non-supplemented groups, whereas citrate excretion was significantly increased (P < 0.05) after the 1st wk only in glycolate and pyridoxine fed rats, when compared to their basal levels. Transaminase activities (GOT [glutamate-oxaloacetate transaminase] and GPT [glutamate-pyruvate transaminase]) of liver, kidney and RBC [red blood cell] decreased significantly with sodium glycolate treatment, but the protective effect by pyridoxine supplementation was seen only in kidney GOT and GPT levels. While administration of such large amounts of pyridoxine alone decreased liver and kidney transaminase activities, the erythrocyte GOT was significantly increased. Apparently, large amounts of pyridoxine fail to lower the hyperoxaluria induced by glycolate feeding rats but this produces changes similar to those observed in pyridoxine deficiency.