Poonkuzhali B, Saraswathi C P, Rajalakshmi K
Department of Biochemistry, Bharathi Women's College, Madras, India.
Indian J Exp Biol. 1994 Jan;32(1):20-4.
Effect of uric acid on sodium oxalate-induced biochemical and histological changes were studied in rats. Rats injected with sodium oxalate (0.7 mg/100 g body wt, ip) show calcium deposits in the lumen of kidney tubules. Uric acid administration was found to potentiate calcium oxalate calculi formation. Lipid peroxide formation was increased up to 100% in kidney and 28% in liver by sodium, oxalate treatment. Uric acid administration was found to reduce lipid peroxide level up to 12% in liver and 20% in kidney. From this study it is concluded that lipid peroxidation may not be the cause of sodium oxalate-induced urolithiasis and the results are discussed with reference to the epitaxic nature of uric acid on kidney stone formation.
在大鼠中研究了尿酸对草酸钠诱导的生化和组织学变化的影响。注射草酸钠(0.7毫克/100克体重,腹腔注射)的大鼠在肾小管管腔内出现钙沉积。发现给予尿酸可增强草酸钙结石的形成。草酸钠处理使肾脏中脂质过氧化物的形成增加高达100%,肝脏中增加28%。发现给予尿酸可使肝脏中脂质过氧化物水平降低高达12%,肾脏中降低20%。从这项研究得出结论,脂质过氧化可能不是草酸钠诱导的尿路结石的原因,并参照尿酸对肾结石形成的取向性质对结果进行了讨论。