Kojima S, Ono H, Kiyozumi M, Honda T, Takadate A
Department of Hygienic Chemistry, Faculty of Pharmaceutical Sciences, Kumamoto University, Japan.
Toxicol Appl Pharmacol. 1989 Mar 15;98(1):39-48. doi: 10.1016/0041-008x(89)90132-4.
The effect of N-benzyl-D-glucamine dithiocarbamate (BGD) on the renal toxicity produced by subacute exposure to cadmium in rats was studied. Rats were injected sc with CdCl2 (1.5 mg Cd/kg) daily for 26 days and thereafter they received 13 injections of BGD (400 mumol/kg) every other day. Urinary protein concentration and AST activity significantly increased after 20 days of cadmium treatment. The pattern of the increase in the urinary excretion of cadmium after cadmium treatment was consistent with that in the urinary excretion of protein and AST. Urinary excretion of amino acid increased gradually after the cessation of cadmium treatment. BGD treatment significantly decreased the urinary excretion of protein, aspartate aminotransferase (AST), and amino acid. Plasma AST activity was elevated 8 days after the beginning of cadmium treatment, indicating that the hepatic damage occurred prior to the renal damage. In addition, the microscopic examination of renal tissue from cadmium-treated rats revealed the necrosis of the proximal tubular cells. The cadmium concentrations in liver and kidney were significantly decreased by BGD treatment. The results of this study indicate that BGD treatment is effective in decreasing the cadmium concentrations in liver and kidney, resulting in the therapeutic effect on the cadmium-induced renal damage.
研究了N-苄基-D-葡糖胺二硫代氨基甲酸盐(BGD)对大鼠亚急性接触镉所致肾毒性的影响。大鼠每天皮下注射CdCl₂(1.5 mg镉/千克),持续26天,此后每隔一天接受13次BGD(400 μmol/千克)注射。镉处理20天后,尿蛋白浓度和AST活性显著升高。镉处理后镉的尿排泄增加模式与蛋白质和AST的尿排泄模式一致。镉处理停止后,氨基酸的尿排泄逐渐增加。BGD处理显著降低了蛋白质、天冬氨酸转氨酶(AST)和氨基酸的尿排泄。镉处理开始8天后,血浆AST活性升高,表明肝损伤先于肾损伤发生。此外,对镉处理大鼠的肾组织进行显微镜检查发现近端肾小管细胞坏死。BGD处理显著降低了肝脏和肾脏中的镉浓度。本研究结果表明,BGD处理可有效降低肝脏和肾脏中的镉浓度,从而对镉诱导的肾损伤产生治疗作用。