Sidhu M, Sharma M, Bhatia M, Awasthi Y C, Nath R
Department of Biochemistry, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Toxicology. 1993 Oct 25;83(1-3):203-13. doi: 10.1016/0300-483x(93)90102-x.
The effect of cadmium (Cd) on the activity of glutathione S-transferase (GST) and glutathione peroxidase (GSH-Px) which play an important role in the detoxification of xenobiotics, was studied in the liver, kidney, heart and lung of Rhesus monkeys. Furthermore, the role of selenium (Se) in the modulation of Cd toxicity with respect to GST and GSH-Px was also evaluated. Cadmium exposure (5 mg Cd/kg body wt./day as CdCl2 for 10 weeks) to monkeys resulted in decreased GSH-Px activity in all four organs present in the order liver > kidney > heart > lung. Cadmium administration also resulted in a significant decrease in total GST activity present in the order liver > heart > kidney > lung, whereas a significant increase in the pi class GST activity was observed greatest in the heart followed by lung, kidney and liver. Oral administration of Se (0.5 mg Se/kg body wt./day as Na2SeO3 for 10 weeks) caused a significant increase in GSH-Px activity in the order liver > heart > kidney > lung. Selenium administration caused an increase in total GST activity in liver and lung but a decrease in kidney and heart. Simultaneous administration of Cd and Se resulted in an increase in total GST activity (except in lung) including the pi class activity as well as GSH-Px activity in all four tissues under study. Thus, the mechanism by which selenium decreases Cd toxicity in Rhesus monkeys, seems to rely on the protection of the enzyme systems GST and GSH-Px in the four organs, possibly by forming non-toxic cadmium selenide.
研究了镉（Cd）对在异生物解毒中起重要作用的谷胱甘肽S-转移酶（GST）和谷胱甘肽过氧化物酶（GSH-Px）活性的影响，实验对象为恒河猴的肝脏、肾脏、心脏和肺。此外，还评估了硒（Se）在调节镉对GST和GSH-Px毒性方面的作用。给猴子暴露镉（以氯化镉形式，5毫克镉/千克体重/天，持续10周）导致所有四个器官中的GSH-Px活性降低，降低顺序为肝脏>肾脏>心脏>肺。给予镉还导致总GST活性显著降低，降低顺序为肝脏>心脏>肾脏>肺，而观察到pi类GST活性显著增加，增加幅度在心脏中最大，其次是肺、肾脏和肝脏。口服硒（以亚硒酸钠形式，0.5毫克硒/千克体重/天，持续10周）导致GSH-Px活性显著增加，增加顺序为肝脏>心脏>肾脏>肺。给予硒导致肝脏和肺中的总GST活性增加，但肾脏和心脏中的总GST活性降低。同时给予镉和硒导致所有四个研究组织中的总GST活性（肺除外）增加，包括pi类活性以及GSH-Px活性增加。因此，硒降低恒河猴镉毒性的机制似乎依赖于保护四个器官中的酶系统GST和GSH-Px，可能是通过形成无毒的硒化镉。
