摘要
在体外实验中,用不同浓度黄磷(0.026μg/ml,0.26μg/ml,2.60μg/ml)与大鼠肝微粒体和线粒体共同孵育,发现黄磷对肝微粒体和线粒体Ca^(2+)-ATP酶呈现抑制作用,且随剂量增大,抑制作用加重;在孵育的早期,对微粒体Ca^(2+)ATP酶的抑制更明显。在整体动物实验中,黄磷染毒后6小时,对肝微粒体和线粒体Ca^(2+)-ATP酶发生抑制。染毒后3小时,对肝微粒体^(45)Ca摄取发生抑制;染毒后6小时,对肝线粒体^(45)Ca摄取发生抑制。实验结果表明,黄磷对微粒体和线粒体Ca^(2+)泵机制的损害可能是引起中毒性肝损害的一个重要因素。
In vitro,rat liver microsome and mitochondria incubated with variousconcentrations of yellow phosporus,showed that their Ca^(2+)-ATPase wereinhibited in a dose-dependant manner.In vivo,the inhibitive role of yellowphopsporus on liver microsome and mitochondria was observed 6h.after dos-ing and the inhibition of Ca^(2+)-uptake of microsome and mitochondria 3h.and6h.after dosing respectively.These results suggested that the impairment ofCalcium-pumps of liver microsome and mitochondria was an important fac-tor in the liver injury induced by yellow phosphorus.
出处
《中华劳动卫生职业病杂志》
CAS
CSCD
1991年第4期216-219,共4页
Chinese Journal of Industrial Hygiene and Occupational Diseases
关键词
黄磷
肝微粒体
线粒体
大鼠
Yellow
Phosphorus
Liver microsome
Liver mitochondria
Ca^(2+)-ATPase
Calcium-uptake
Toxic liver injury
