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首页> 外文期刊>Journal of biochemical and molecular toxicology >Protection against acetaminophen hepatotoxicity by clofibrate pretreatment: Role of catalase induction.
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Protection against acetaminophen hepatotoxicity by clofibrate pretreatment: Role of catalase induction.

机译：氯贝特预处理可预防对乙酰氨基酚肝毒性：过氧化氢酶诱导作用。

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摘要

Mice pretreated with the peroxisome proliferator clofibrate (CFB) are highly resistant to acetaminophen (APAP)-induced hepatotoxicity. The objective of the present study was to investigate whether the increase in hepatic catalase activity following CFB pretreatment plays a role in this hepatoprotection. An irreversible inhibitor, 3-amino-1,2,4-triazole (3-AT), was used to modulate catalase activity. Hepatic catalase activity in mice pretreated with CFB (500 mg/kg, i.p., for 10 days) was significantly inhibited by 3-AT (100 or 500 mg/kg, i.p.). In addition, the lower dose of 3-AT (100 mg/kg) had minimal effect on biliary and urinary excretion of APAP metabolites generated from a nontoxic dose, suggesting that APAP metabolism was not modulated by this dose of 3-AT. The mortality rate of corn-oil-pretreated mice challenged with APAP (800 mg/kg, p.o.) was significantly increased by 3-AT (100 mg/kg, i.p.) given 1 h before APAP. As expected, CFB pretreatment conferred full protection against APAP-induced hepatotoxicity. The same 3-AT treatment, however, did not abolish hepatoprotection in CFB-pretreated mice, despite the marked inhibition of hepatic catalase activity. In conclusion, these results indicate that elevated catalase activity in mice exposed to CFB does not appear to mediate the hepatoprotection, suggesting that other cellular defense mechanisms are involved.
机译：用过氧化物酶体增殖物clofibrate（CFB）预处理的小鼠对乙酰氨基酚（APAP）诱导的肝毒性具有高度抗性。本研究的目的是研究CFB预处理后肝过氧化氢酶活性的增加是否在这种保肝中起作用。使用不可逆抑制剂3-氨基-1,2,4-三唑（3-AT）调节过氧化氢酶活性。 3-AT（100或500 mg / kg，i.p.）显着抑制了CFB预处理（500 mg / kg，i.p.，10天）小鼠的肝过氧化氢酶活性。此外，较低剂量的3-AT（100 mg / kg）对无毒剂量产生的APAP代谢产物的胆汁和尿液排泄影响最小，表明该剂量的3-AT不会调节APAP代谢。在APAP前1小时给予3-AT（100 mg / kg，i.p.）的APAP（800 mg / kg，p.o.）攻击的玉米油预处理小鼠的死亡率显着提高。不出所料，CFB预处理可提供针对APAP诱导的肝毒性的全面保护。尽管对肝过氧化氢酶活性有明显的抑制作用，但是相同的3-AT处理并未消除CFB预处理小鼠的肝保护作用。总之，这些结果表明，暴露于CFB的小鼠中过氧化氢酶活性的升高似乎并未介导肝保护作用，这表明还涉及其他细胞防御机制。

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