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首页> 外文期刊>The Journal of toxicological sciences >Carbon tetrachloride-induced lethality in mouse is prevented by multiple pretreatment with zinc sulfate
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Carbon tetrachloride-induced lethality in mouse is prevented by multiple pretreatment with zinc sulfate

机译：硫酸锌多次预处理可防止四氯化碳诱导的小鼠致死性

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Carbon tetrachloride (CCl4) is commonly used as a chemical inducer of experimental liver injury. Several compounds have been demonstrated to attenuate the hepatic damage caused by sublethal doses of CCl4. However, rescue from lethal toxicity of CCl4 has not been reported. In the present study, we evaluated the protective effect of metallothionein (MT), an endogenous scavenger of free radicals, on CCl4-induced lethal toxicity of mice. To induce MT production in male ddY mice, we administered Zn (as ZnSO4) at 50 mg/kg as a once-daily subcutaneous injection for 3 days prior to a single intraperitoneal administration of 4 g/kg CCl4. Animals were observed for mortality every 3 hr for 24 hr after CCl4 injection. Liver damage was assessed by determining (in a subset of these mice) blood levels of alanine aminotransferase (ALT; a marker of liver injury) and liver histopathology at 6 hr after CCl4 injection. Our results showed that three times pretreatment with Zn yielded > 40-fold induction of hepatic MT protein levels compared to control group. Zn pretreatment completely abolished the CCl4-induced mortality of mice. We also found that pretreatment of mice with Zn significantly decreased the ALT levels and reduced the histological liver damage as assessed at 6 hr post-CCl4. These findings suggest that prophylaxis with Zn protects mice from CCl4-induced acute hepatic toxicity and mortality, presumably by induction of radical-scavenging MT.
机译：四氯化碳（CCl4）通常用作实验性肝损伤的化学诱导剂。已证明几种化合物可减轻亚致死剂量的CCl4引起的肝损伤。但是，尚未报道从CCl4的致命毒性中解救出来的方法。在本研究中，我们评估了内源性自由基清除剂金属硫蛋白（MT）对CCl4诱导的小鼠致死毒性的保护作用。为了在雄性ddY小鼠中诱导MT产生，我们在一次腹膜内施用4 g / kg CCl4之前，以每天一次皮下注射的方式，以每天一次皮下注射的方式，以50 mg / kg的剂量施用Zn（作为ZnSO4）。注射CCl 4后每24小时每3小时观察一次动物死亡率。通过在注射CCl4后6小时（在这些小鼠的子集中）确定丙氨酸转氨酶（ALT;肝损伤的标志物）的血液水平和肝脏组织病理学，评估肝损伤。我们的结果表明，与对照组相比，锌的三倍预处理可诱导> 40倍的肝MT蛋白水平诱导。锌预处理完全消除了CCl4诱导的小鼠死亡率。我们还发现，如在CCl4后6小时评估，用Zn预处理小鼠可显着降低ALT水平并减少组织学肝损伤。这些发现表明，锌的预防可以保护小鼠免受CCl4诱导的急性肝毒性和死亡的影响，大概是通过诱导自由基清除MT引起的。

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