Sentürk U K, Oner G, Izgüt-Uysal V M
Akdeniz University, Faculty of Medicine, Department of Physiology, Antalya, Turkey.
J Basic Clin Physiol Pharmacol. 1994 Jul-Dec;5(3-4):305-13. doi: 10.1515/jbcpp.1994.5.3-4.305.
Since the kidney is the main target organ for many metals including cadmium, the generation of the products of lipid peroxidation due to accumulation of these toxic metals in the kidney may have importance in the mechanism of their nephrotoxicity. In order to test this hypothesis, we carried out an experimental study in rats. The functions and the levels of tiobarbituric acid reactive substances (TBARS) of the kidney were investigated in animals receiving 15 micrograms/ml aqueous Cd solution for 30 days. Due to cadmium accumulation in kidney cortex, the ratio of Cd/Zn increased significantly and this increase was associated with elevated TBARS in both renal cortex and medulla. The content of TBARS in renal cortex rose from 211.6 +/- 64.2 to 303.4 +/- 46.4 nmol/g protein (p<0.01) and GFR decreased to 390.5 +/- 109.4 from 1008.7 +/- 4.8 microliters/min (p<0.01) in cadmium exposed animals. Daily coadministration of selenium, vitamins A, C, E did not reverse the adverse effect of cadmium on kidney function, despite the significant decrease in cortex TBARS levels (p<0.01). In conclusion, these data suggest to us that lipid peroxidation assessed by TBA test may not be the only mechanism in cadmium induced nephrotoxicity.
由于肾脏是包括镉在内的许多金属的主要靶器官，这些有毒金属在肾脏中积累导致脂质过氧化产物的生成可能在其肾毒性机制中具有重要意义。为了验证这一假设，我们在大鼠身上进行了一项实验研究。对接受15微克/毫升镉水溶液30天的动物的肾脏功能和硫代巴比妥酸反应性物质（TBARS）水平进行了研究。由于镉在肾皮质中积累，镉/锌的比值显著增加，且这种增加与肾皮质和髓质中TBARS的升高有关。镉暴露动物的肾皮质中TBARS含量从211.6±64.2纳摩尔/克蛋白质升至303.4±46.4纳摩尔/克蛋白质（p<0.01），肾小球滤过率从1008.7±4.8微升/分钟降至390.5±109.4微升/分钟（p<0.01）。尽管皮质TBARS水平显著降低（p<0.01），但每日同时给予硒、维生素A、C、E并不能逆转镉对肾功能的不良影响。总之，这些数据表明，通过TBA试验评估的脂质过氧化可能不是镉诱导肾毒性的唯一机制。
