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给大鼠注射异丙嗪以及使用四氯化碳会诱导肝微粒体脂质的脂质过氧化。

Promethazine administration to rats and CCl4 induced lipid peroxidation of liver microsomal lipids.

作者信息

de Toranzo E G, Marzi A, Castro J A

出版信息

Res Commun Chem Pathol Pharmacol. 1980 Oct;30(1):91-8.

PMID:7433770
Abstract

Promethazine inhibited CCl4 stimulated microsomal lipid peroxidation in vitro at concentrations ranging from 10(-3) to 10(-8)M. CCl4 administered to rats at a dose of 1 ml/kg decreased the arachidonic acid content of microsomal lipids after 6 hours of intoxication. Prior promethazine treatment, at dosage regimes that preclude CCl4 induced liver necrosis at 24 hours, did not significantly prevent the CCl4 induced decrease in arachidonic acid content. Moreover, promethazine itself produced a similar decrease but in complete absence of liver damage. Results suggest that either lipid peroxidation is not relevant to liver injury or that the arachidonic acid decrease in microsomal lipids is not evidence for lipid peroxidation occurrence or that promethazine effects are not related to inhibition of lipid peroxidation.

摘要

异丙嗪在体外浓度范围为10⁻³至10⁻⁸M时可抑制四氯化碳刺激的微粒体脂质过氧化。以1 ml/kg的剂量给大鼠注射四氯化碳,中毒6小时后微粒体脂质的花生四烯酸含量降低。事先进行异丙嗪治疗,在24小时可防止四氯化碳诱导肝坏死的剂量方案下,并未显著阻止四氯化碳诱导的花生四烯酸含量降低。此外,异丙嗪本身也产生了类似的降低,但完全没有肝损伤。结果表明,要么脂质过氧化与肝损伤无关,要么微粒体脂质中花生四烯酸的降低不是脂质过氧化发生的证据,要么异丙嗪的作用与脂质过氧化的抑制无关。

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