Stajn A, Zikić R V, Ognjanović B, Saicić Z S, Pavlović S Z, Kostić M M, Petrović V M
Faculty of Sciences, University of Kragujevac, Yugoslavia.
Comp Biochem Physiol C Pharmacol Toxicol Endocrinol. 1997 Jun;117(2):167-72. doi: 10.1016/s0742-8413(97)00063-7.
To examine effects of exogenous Cd on the kidney antioxidant defense system (AOS) and the possible protective role of Se against Cd toxicity, male Wistar albino rats (2 months old) were exposed during 30 days to oral intake of 200 ppm Cd (as CdCl2), 0.l ppm Se (as Na-selenite) or to the same doses of Cd / Se, simultaneously. Marked accumulation of Cd (23.44 +/- 0.69 micrograms/g w.m.) and marked alterations of AOS, resulting in kidney injury (renal pseudohypertrophy), were found in Cd-treated rats. Activities of total superoxide dismutase (SOC, EC 1.15.1.1), manganese-containing superoxide dismutase (MnSOD) and selenium-dependent glutathione peroxidase (Se GSH-Px, EG 1.11.1.9) were significantly reduced, whereas that of glutathione-S-transferase (CST, EC 2.5.1.18) and vitamin E (vit E) concentration were significantly increased in the kidneys of Cd-treated rats. Kidney catalase (CAT, EC 1.11.1.6) activity, ascorbic acid (AsA) and red blood cell glutathione (GSH, GSSG) levels were not markedly influenced by CD uptake. In kidneys of Se treated rats, the activities of total SOD, copper-zinc-containing superoxide dismutase (CuZnSOD) and GST were significantly increased Activities of kidney CAT and Se GSH-Px were largely unchanged, whereas significant increases of the kidney AsA and vit E concentrations occurred. In Cd + Se-cotreated rats, the kidney activities of MnSOD, CAT and Se GSH-Px, as well as vit E concentration, were the same as in controls, whereas CuZnSOD and GST activities and concentration of AsA exceeded normal values. These data indicate that Se only partially improves the AOS that is insufficient to prevent Cd-induced nephrotoxicity.
为研究外源性镉对肾脏抗氧化防御系统（AOS）的影响以及硒对镉毒性的可能保护作用，将2月龄雄性Wistar白化大鼠经口摄入200 ppm镉（以CdCl₂形式）、0.1 ppm硒（以亚硒酸钠形式）或相同剂量的镉/硒，同时处理30天。在镉处理的大鼠中发现镉显著蓄积（23.44±0.69微克/克湿重）以及AOS显著改变，导致肾脏损伤（肾假性肥大）。镉处理大鼠肾脏中总超氧化物歧化酶（SOC，EC 1.15.1.1）、含锰超氧化物歧化酶（MnSOD）和硒依赖性谷胱甘肽过氧化物酶（Se GSH-Px，EG 1.11.1.9）的活性显著降低，而谷胱甘肽-S-转移酶（CST，EC 2.5.1.18）的活性和维生素E（vit E）浓度显著升高。肾脏过氧化氢酶（CAT，EC 1.11.1.6）活性、抗坏血酸（AsA）和红细胞谷胱甘肽（GSH，GSSG）水平未受镉摄入的显著影响。在硒处理的大鼠肾脏中，总SOD、含铜锌超氧化物歧化酶（CuZnSOD）和GST的活性显著增加。肾脏CAT和Se GSH-Px的活性基本未变，而肾脏AsA和vit E浓度显著增加。在镉+硒联合处理的大鼠中，肾脏MnSOD、CAT和Se GSH-Px的活性以及vit E浓度与对照组相同，而CuZnSOD和GST的活性以及AsA浓度超过正常值。这些数据表明，硒仅部分改善了不足以预防镉诱导的肾毒性的AOS。
