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消草磷与经苯巴比妥预处理大鼠的肝微粒体一起温育,在有NADPH存在时,最多可使肝微粒体细胞色素P450丢失58％左右。苯巴比妥预处理大鼠经ip或po 1.0g/kg消草磷,18h后肝微粒体P450将丢失40％左右,但用还原态P450甲吡酮络合物生成量估算剩余P450的亚族组成却无显著变化。此现象似提示消草磷的体内活性代谢物之一或许是硫化氢。尽管高剂量消草磷体内与体外均导致P450破坏,但低剂量(如 0.1g/kg)短期接触却不致诱发以肝脏P450丢失为特征的特殊肝脏毒性。
Phosphatidylinositol is incubated with liver microsomes pretreated with phenobarbital in rats, where up to 58% of liver microsomal cytochrome P450 can be lost in the presence of NADPH. Phenobarbital pretreatment of rats with ip or po 1.0g / kg eliminate phosphorus, liver microsomal P450 18h will be lost about 40%, but the use of reduced P450 metyrapone complex formation estimate of the remaining P450 There was no significant change in ethnic composition. This phenomenon seems to suggest that one of the active metabolites in the body that may be excreted by phosphorus is hydrogen sulfide. Short-term exposure to low doses (eg, 0.1 g / kg) did not induce specific liver toxicity characterized by loss of liver P450, although P450 was caused both in vitro and in vivo at high doses.