去铁胺在实验性肝损伤中的解毒作用——脂质过氧化的作用

Antidotal effects of deferrioxamine in experimental liver injury--role of lipid peroxidation.

作者信息

Siegers C P, Steffen B, Younes M

机构信息

Institute of Toxicology, Medical University of Lübeck, Federal Republic of Germany.

出版信息

Pharmacol Res Commun. 1988 Apr;20(4):337-43. doi: 10.1016/s0031-6989(88)80070-5.

DOI:10.1016/s0031-6989(88)80070-5

PMID:3387462

Abstract

Pretreatment with deferrioxamine (DFO, 125-500 mg/kg i.p.) protected male mice against CCl4- or CBrCl3-induced hepatotoxicity which is closely related to an inhibition of iron-dependent lipid peroxidation monitored by ethane exhalation. For allyl alcohol, 1,1-dichloroethylene, dimethylnitrosamine, thioacetamide, bromobenzene and paracetamol no hepatoprotection was achieved with DFO indicating that lipid peroxidation is not involved as a primary mechanism of toxicity. In the case of bromobenzene a marked in vivo lipid peroxidation was observed, which was unaffected by DFO and appears therefore to be iron-dependent.

摘要

用去铁胺（DFO，腹腔注射125 - 500 mg/kg）预处理可保护雄性小鼠免受四氯化碳或三溴氯甲烷诱导的肝毒性，这与通过乙烷呼出量监测的铁依赖性脂质过氧化的抑制密切相关。对于烯丙醇、1,1 - 二氯乙烯、二甲基亚硝胺、硫代乙酰胺、溴苯和对乙酰氨基酚，DFO未实现肝保护，表明脂质过氧化不是主要的毒性机制。在溴苯的情况下，观察到明显的体内脂质过氧化，其不受DFO影响，因此似乎是铁依赖性的。