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谷胱甘肽及其酶系与黄磷毒作用关系研究
引用本文:陈哲生,周炯亮. 谷胱甘肽及其酶系与黄磷毒作用关系研究[J]. 毒理学杂志, 1990, 0(1)
作者姓名:陈哲生  周炯亮
作者单位:中山医科大学卫生学院,中山医科大学卫生学院 广东省卫生防疫站毒理室
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。

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

Interation among GSH, GSH enzymes Metabolism and Phosphorus Poisoning
Chen Zhesheng,Zhou Jiongliang. Interation among GSH, GSH enzymes Metabolism and Phosphorus Poisoning[J]. Journal of Toxicology, 1990, 0(1)
Authors:Chen Zhesheng  Zhou Jiongliang
Abstract: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.
Keywords:P4  GSH enzymes  OTC  BS(?).
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