摘要
本文综合报告了五氧化二钒、顺铂、四氯化碳和氯丁二稀(CBD)引起肾或肝损害的氧化应激机理的研究结果。体内外试验显示,V_2O_5引起肾皮质及其微粒体丙二醛(MDA)增高和(或)膜流动性下降。顺铂引起肾皮质GSH耗竭、葡糖异生作用抑制及MDA增高。CCl_4和CBD引起肝细胞色素P450量下降、抗氧化物质耗竭、MDA增高、膜损害及钙但稳失调。上述结果提示这四种化学物所致靶器官损害在不同程度上与氧化应激有关。本文还报告了某些化学品对这些毒物引起的氧化应激和损伤的防护作用。
Oxidative stress mechanism of liver or kidney damages indued by vanadium pentoxide (V2O3), cisplatin ( CDDP ), carbon tetrachloride ( CCl8 ) and chloroprene ( CBD ) in vitro and in vivo has been investigated recently in our laboratory. V3O5 increased formation of lipid peroxide in rat kidney cortical homogenates and microsomes and decreased membrane lipid fluidity of microsomes. CDDP resultd in depletion of glutathione, inhibition of gluc- onogenesis and increase of malondialdehyde ( MDA ) in rat kidney cortex. CCl4 and CBD caused decrease of content of cytochrome P450, depletion of antioxidants, increase of MDA, damages of membranes and disruption of intracellular calcium homeostasis in rat liver in vivo or in vitro. These findings suggest that kidney or liver injuries indued by V2O5, CDDP, CCl4 and CBD in rats may be associated with reactive intermediate formation and subsequent oxldative stress to different extent. Moreover, the protective effects of some chemicals on the oxidative stress and damage induced by these toxicants in rats were studied in this paper.
出处
《卫生毒理学杂志》
CSCD
1992年第2期82-83,81,共3页
Journal of Health Toxicology
关键词
氧化应激
化学物质
中毒
毒理学
Vanadium pentoxide
Cisplatin
Carbon tetrachloride
Chloroprene
Oxidati-ve stress.
