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硒对阿霉素诱导的肝脏线粒体功能障碍的恢复作用。

Recovery of adriamycin induced mitochondrial dysfunction in liver by selenium.

作者信息

Taskin E, Dursun N

机构信息

Department of Physiotherapy and Rehabilitation, School of Health Sciences, Istanbul Bilim University, Yazarlar Sokak No: 17, Esentepe-Şişli, 34394, Istanbul, Turkey.

Department of Physiology, Faculty of Medicine, University of Erciyes, Kayseri, Turkey.

出版信息

Cytotechnology. 2015 Dec;67(6):977-86. doi: 10.1007/s10616-014-9736-x. Epub 2014 Oct 18.

DOI:10.1007/s10616-014-9736-x
PMID:25322894
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4628925/
Abstract

Adriamycin (ADR) is a chemotherapeutic drug. Its toxicities may associate with mitochondriopathy. Selenium (Se) is a trace element for essential intracellular antioxidant enzymes. However, there is lack of data related to the effect of selenium on the liver tissue of ADR-induced mitochondrial dysfunction. The study was to investigate whether Se could restore mitochondrial dysfunction of liver-exposed ADR. Rats were divided into four groups as a control, ADR, Se, co-treated ADR with Se groups. The biochemical measurements of the liver were made in mitochondrial and cytosol. ATP level and mitochondria membrane potential (MMP) were measured. Total oxidant (TOS), total antioxidant (TAS) status were determined and oxidative stress index (OSI) was calculated by using TOS and TAS. ADR increased TOS in mitochondria and also oxidative stress in mitochondria. ADR sligtly decreased MMP, and ATP level. Partial recovery of MMP by Se was able to elevate the ATP production in cotreatment of ADR with Se. TOS in mitochondria and cytosol was diminished, as well as OSI. We concluded that selenium could potentially be used against oxidative stress induced by ADR in liver, resulting from the restoration of MMP and ATP production and prevention of mitochondrial damage in vivo.

摘要

阿霉素(ADR)是一种化疗药物。其毒性可能与线粒体病有关。硒(Se)是细胞内必需抗氧化酶的一种微量元素。然而,缺乏关于硒对阿霉素诱导的线粒体功能障碍肝脏组织影响的数据。该研究旨在调查硒是否能恢复暴露于阿霉素的肝脏的线粒体功能障碍。大鼠被分为四组:对照组、阿霉素组、硒组、阿霉素与硒联合治疗组。对肝脏进行线粒体和胞质溶胶的生化检测。测量ATP水平和线粒体膜电位(MMP)。测定总氧化剂(TOS)、总抗氧化剂(TAS)状态,并使用TOS和TAS计算氧化应激指数(OSI)。阿霉素增加了线粒体中的TOS以及线粒体中的氧化应激。阿霉素轻微降低了MMP和ATP水平。硒对MMP的部分恢复能够在阿霉素与硒联合治疗中提高ATP的产生。线粒体和胞质溶胶中的TOS以及OSI均降低。我们得出结论,硒可能对阿霉素在肝脏中诱导的氧化应激具有潜在的对抗作用,这是由于其恢复了MMP和ATP的产生,并在体内预防了线粒体损伤。

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本文引用的文献

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Ren Fail. 2014 May;36(4):606-12. doi: 10.3109/0886022X.2014.882737. Epub 2014 Feb 6.
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NAD(+) administration decreases doxorubicin-induced liver damage of mice by enhancing antioxidation capacity and decreasing DNA damage.烟酰胺腺嘌呤二核苷酸(NAD(+))的补充可以通过增强抗氧化能力和减少 DNA 损伤来降低阿霉素诱导的小鼠肝损伤。
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Quercetin-induced cardioprotection against doxorubicin cytotoxicity.槲皮素对抗阿霉素细胞毒性的心脏保护作用。
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Models of hepatotoxicity and the underlying cellular, biochemical and immunological mechanism(s): a critical discussion.肝毒性模型及其潜在的细胞、生化和免疫机制:批判性讨论
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