Department of Pharmaceutical Technology, Division of Biochemistry, Jadavpur University, P.O. Box 17028, Calcutta 700 032, India.
Environ Toxicol Pharmacol. 1998 Nov 1;6(3):201-7. doi: 10.1016/s1382-6689(98)00035-0.
In the present investigation a time-responsive oxidative stress, both in liver and kidney were carried out following cadmium (Cd) exposure. Cadmium was administered subcutaneously on each other day in normal saline solution. Mice were sacrificed on the 15th, 30th and 45th days post-exposure. For oxidative stress study different biochemical markers, e.g. lipid peroxidation (LPO), reduced glutathione (GSH) and glutathione S-transferase (GST) activity were considered. Time-responsive exponential increase in the lipid peroxidation and decrease in glutathione level and glutathione S-transferase activity occurred both in hepatic and renal tissues following cadmium treatment. Though both the organs responded in a similar fashion, their magnitude of response was found to be different. Body weight did not differ but relative liver and kidney weight were found to be significantly increased at different time points. The possible mechanism of time-dependent cadmium-induced toxic effects and relation between hepatic and renal biochemical response have been discussed.
本研究在镉(Cd)暴露后对肝脏和肾脏进行了时间依赖性氧化应激研究。镉以生理盐水溶液的形式每隔一天皮下给药。在暴露后的第 15、30 和 45 天处死小鼠。为了进行氧化应激研究,考虑了不同的生化标志物,例如脂质过氧化 (LPO)、还原型谷胱甘肽 (GSH) 和谷胱甘肽 S-转移酶 (GST) 活性。镉处理后,肝脏和肾脏组织中的脂质过氧化呈时间依赖性指数增加,谷胱甘肽水平和谷胱甘肽 S-转移酶活性降低。尽管两个器官的反应方式相似,但发现它们的反应幅度不同。体重没有差异,但在不同时间点发现肝脏和肾脏的相对重量显著增加。讨论了时间依赖性镉诱导的毒性作用的可能机制以及肝肾功能的生化反应之间的关系。