谷胱甘肽及其酶系与黄磷毒作用关系研究  

Interation among GSH,GSH enzymes Metabolism and Phosphorus Poisoning

作　　者：陈哲生[1,2] 周炯亮[1] 

机构地区：[1]中山医科大学卫生学院 [2]广东省卫生防疫站毒理室

出　　处：《卫生毒理学杂志》1990年第1期18-20,共3页Journal of Health Toxicology

摘　　要：黄磷急性染毒可使肝脏GSH含量降低,染毒60小时后肝GSR明显抑制,肝GST在染毒早期有诱导倾向,24小时后转为抑制。OTC预处理可明显增加肝GSH含量,缓解黄磷所致的肝GSH降低和血清γ-GT的升高。BSO预处理能明显减少肝GSH含量,加剧黄磷所致的肝GSH降低及血清γ-GT的升高。黄磷亚急性染毒对肝GSH及其代谢酶系影响甚微。Acute P4 poisoning decreased the hepatic GSH content. The activities of hepatic Glutathion redutase ( GSR ) and Glutathion-S-transferases ( GST ) were inhibited 6 and 24 hours after P4 were given respectively. Hepatic GSH content was obviously increased due to pretreatment with L-2 oxo-thiazolidine-4-carboxylate ( OTC ) suggesting that OTC wound probably protest liver against the toxicity of P4. Hepatic GSH content was remarkably decreased due to pretreatment with Bu thionine sulfoxinine ( BSO ) suggesting that BS) might potentiate the toxicity of P,. However subacute P4 poisoning had little effect on GSH metabolism.

关 键 词：黄磷 谷胱甘肽酶系 L-2-氧-4-氢噻唑-4-羧酸盐 DL-甲硫氨酸磺酰亚胺 

分 类 号：R994.3[医药卫生—毒理学]