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氧化应激:铅诱导细胞凋亡和肾毒性的可能机制。

Oxidative stress: a possible mechanism for lead-induced apoptosis and nephrotoxicity.

机构信息

Experimental Center of Medicine, Lanzhou General Hospital of Lanzhou Military, People's Liberation Army, Key Laboratory of Stem Cells and Gene Drug of Gansu Province, 333 Southern Binhe Road, Lanzhou 730050, China.

出版信息

Toxicol Mech Methods. 2012 Nov;22(9):705-10. doi: 10.3109/15376516.2012.718811. Epub 2012 Aug 31.

DOI:10.3109/15376516.2012.718811
PMID:22894711
Abstract

Lead-induced nephrotoxicity is a human health hazard problem. In this study, Human mesangial cells (HMCs) were treated with different concentration of lead acetate (5, 10, 20 μmol/l) in order to investigate the oxidative stress and apoptotic changes. It was revealed that lead acetate could induce a progressive loss in HMCs viability together with a significant increase in the number of apoptotic cells using 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl tetrazolium (MTT) assay and flow cytometry, respectively. The apoptotic morphological changes induced by lead exposure in HMCs were demonstrated by PI-Hochest33342 staining. A DNA laddering pattern in lead-treated cells was shown, which could indicate nuclear fragmentation. In addition, lead acetate significantly increased the levels of malondialehyde (MDA) content and lactate dehydrogenase (LDH) activity. Therefore, it might be concluded that lead could promote HMCs' oxidative stress and apoptosis, which may be the chief mechanisms of lead-induced nephrotoxicity.

摘要

铅诱导的肾毒性是一个对人类健康有害的问题。在这项研究中,用人肾小球系膜细胞(HMCs)分别用不同浓度的醋酸铅(5、10、20μmol/L)处理,以研究氧化应激和细胞凋亡的变化。结果表明,醋酸铅可诱导 HMCs 活力进行性丧失,同时用 3-(4,5-二甲基-2-噻唑基)-2,5-二苯基四氮唑(MTT)法和流式细胞术分别检测到凋亡细胞数量显著增加。碘化丙啶(PI)-Hochest33342 染色显示铅暴露诱导的 HMCs 凋亡形态变化。在铅处理的细胞中出现了 DNA 梯状图案,这可能表明核片段化。此外,醋酸铅显著增加了丙二醛(MDA)含量和乳酸脱氢酶(LDH)活性。因此,可以得出结论,铅可能促进 HMCs 的氧化应激和凋亡,这可能是铅诱导肾毒性的主要机制。

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