大鼠肝脏混合功能氧化酶系在黄磷肝损伤中的变化特点和作用

Changes of the Role of Hepatic MFOs Fu nctions in Yellow Phosphorus Poisoned Rats

雄性SD大鼠按1、3和6mg/kg急性经口给予黄磷,24小时后肝脏P_(450)、b_5和苯胺羟化酶在3和6mg/kg组出现抑制并随时间延长而抑制增加1mg/kg组则出现阶段性升高:另外动物每周按2mg/kg染磷5周,脱甲基酶在早期升高,苯胺羟化酶在后期升高,P_(450)变化不大,b_5在后期出现降低。苯巴比妥预处理动物可以明显增加黄磷的肝毒性,除肝中甘油三酯、血清r-GT和SGPT大幅度提高外,尚有明显的坏死灶出现。实验结果提示黄磷可以影响体内的混合功能氧化酶系统并在该系统代谢后可能转变成毒性较原型为大的代谢物。黄磷诱导差示光谱显示在415nm处出现一个明显的负吸收峰,但在380nm处附近未见新的吸收峰。文章还对黄磷影响MFO系统的可能机理进行了探讨。

Male SD rats were fed orally with 1,3 or 6mg/kg of yellow phosphor-us(P),which resulted,after 24 h,in a decrease of liver P_(450),b_5 and aniline hydroxylase (AH) in the 3 and 6mg/kg groups,but increased peri-odically in the 1mg/kg group.When fed with a dose of 2mg/kg/week for five weeks,Aminopyrine-N-demethylase was elevated in the ear-lier stage,whereas AH was elevated and b_5lowered in the later stage.No evident change of p_(450) was observed.Pretreatment with phenobarbital enhanced while CoCl_2 alleviated the toxicity of P.These results sug-gested that P could produce more injuries to hepatocytes after metabolized by MFOs.Repetitive scaanning of different spectra from 550nm to350nm during P oxidation by rat liver microsomes showed that λmax was stillat the same level of the base line and λmin was at 415nm.