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硒对体内铝诱导的小鼠肝脏氧化应激的保护作用。

Protective effect of selenium on aluminium-induced oxidative stress in mouse liver in vivo.

机构信息

Department of Biochemistry, Kaunas University of Medicine, Mickeviciaus 9, LT-44307 Kaunas, Lithuania.

出版信息

Environ Toxicol Pharmacol. 2011 Mar;31(2):302-6. doi: 10.1016/j.etap.2010.11.008. Epub 2010 Nov 27.

Abstract

The aim of the study was to evaluate possible protective effects of selenium (Se) against systemic aluminium (Al) toxicity and the redox status of mouse liver after short-term (16 h) exposure to Al in vivo. BALB/c mice were injected i.p. with AlCl(3) (25mg Al(3+) per kg of body mass) or/and Na(2)SeO(3) (1.25mg Se per kg of body mass). The 4-fold increased activity of ALT in serum showed systemic hepatotoxicity that Se could not prevent by competitive mechanisms. The protective effects of Se could only be observed on intracellular oxidative stress events as determined by glutathione status. Exposure to Al leads to the decrease in the total glutathione (GSH(tot)) and GSH/GSSG redox ratio to about 50% of the control. Upon co-exposure to Se+Al, the concentration of GSH(tot) and the redox ratio was restored to the control values. Our results indicate that Se did not have a protective effect on Al-linked liver toxicity, but did ameliorate intracellular oxidative stress processes mediated by glutathione.

摘要

本研究旨在评估硒 (Se) 对短期(16 小时)体内暴露于铝 (Al) 后小鼠肝脏全身 Al 毒性和氧化还原状态的可能保护作用。BALB/c 小鼠经腹腔注射 AlCl3(每公斤体重 25mg Al3+)和/或 Na2SeO3(每公斤体重 1.25mg Se)。血清中 ALT 活性增加 4 倍表明存在系统性肝毒性,而 Se 不能通过竞争机制来预防。只有当观察到细胞内氧化应激事件时,才能观察到 Se 的保护作用,这可以通过谷胱甘肽状态来确定。暴露于 Al 会导致总谷胱甘肽 (GSH(tot)) 和 GSH/GSSG 氧化还原比降低至对照的约 50%。当同时暴露于 Se+Al 时,GSH(tot) 的浓度和氧化还原比恢复到对照值。我们的结果表明,Se 对与 Al 相关的肝毒性没有保护作用,但可改善由谷胱甘肽介导的细胞内氧化应激过程。

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