The study was conducted to investigate the effect of vitamin A, B₁ and B₆ deficiency on oxalate metabolism in rats. A significant hyperoxaluria was the common observation in all the three vitamin deficiencies (vitamin B₆> vitamin A > vitamin B₁). The activities of hepatic glycolate oxidase and glycolate dehydrogenase were markedly enhanced in vitamin-A- and vitamin-B₆-deficient rats. However, lactate dehydrogenase levels remained unaltered in these deficiencies as compared to their respective pair-fed controls. Vitamin B₁ deficiency of 4 weeks’ duration could augment the activity of glycolate oxidase only, with no alterations in the glycolate dehydrogenase and lactate dehydrogenase levels. Intestinal oxalate uptake studies revealed increased bio-availability of oxalate from the gut in vitamin-A- and vitamin-B₆-deficient rats. Thus, the results suggest the relative contribution of both exogenous as well as endogenous oxalate in the process of calculogenesis under various nutritional stress conditions in rat.

No abstract

No abstract

No abstract

SummaryThe intestinal uptake of [14C]oxalate, [14C] glyoxylate, and [14C] glycolate are studied in brush border membrane vesicles (BBMV) isolated from vitamin A-deficient and pair-fed control rats. The data obtained indicate that oxalate and its precursors are transported across the BBMV by passive diffusion. The intestinal uptake of glyoxylate and glycolate remains unaltered in vitamin A deficiency, while uptake rate of oxalate was significantly increased (p<0.01) in vitamin A-deficient rats as compared to pair-fed controls. In conclusion, the results indicate that vitamin A deficiency leads to hyperabsorption of oxalate through the gut.