Sharma S, Sidhu H, Narula R, Thind S K, Nath R
Department of Biochemistry, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Ann Nutr Metab. 1990;34(2):104-11. doi: 10.1159/000177576.
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 greater than vitamin A greater than 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.
本研究旨在探讨维生素A、B1和B6缺乏对大鼠草酸代谢的影响。在所有三种维生素缺乏（维生素B6缺乏＞维生素A缺乏＞维生素B1缺乏）的情况下，均观察到明显的高草酸尿症。在维生素A和维生素B6缺乏的大鼠中，肝脏乙醇酸氧化酶和乙醇酸脱氢酶的活性显著增强。然而，与各自的配对喂养对照组相比，这些缺乏情况下乳酸脱氢酶水平保持不变。持续4周的维生素B1缺乏仅能增强乙醇酸氧化酶的活性，而乙醇酸脱氢酶和乳酸脱氢酶水平无变化。肠道草酸摄取研究表明，维生素A和维生素B6缺乏的大鼠肠道中草酸的生物利用度增加。因此，结果表明在大鼠各种营养应激条件下，外源性和内源性草酸在结石形成过程中都有相对贡献。
