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胆红素对细胞的氧化还原状态、氧化应激以及保护和毒性作用的分子机制。

Redox state, oxidative stress, and molecular mechanisms of protective and toxic effects of bilirubin on cells.

作者信息

Tell Gianluca, Gustincich Stefano

机构信息

Department of Biomedical Sciences and Technologies, University of Udine, Italy.

出版信息

Curr Pharm Des. 2009;15(25):2908-14. doi: 10.2174/138161209789058174.

DOI:10.2174/138161209789058174
PMID:19754367
Abstract

Unconjugated bilirubin (UCB) is the major degradation product of the heme catabolism. UCB is a potent antioxidant molecule as well as an indirect pro-oxidant generator. Growing evidence suggests that its major cellular effects are mediated by inhibiting proliferation in cancer cell lines and eliciting cytotoxicity, particularly in neurons and glial cells. Here we describe studies showing that alteration of the redox status and generation of oxidative stress are likely early events responsible for UCB-induced cytotoxicity. We then elucidate some of the molecular pathways that govern these effects.

摘要

未结合胆红素(UCB)是血红素分解代谢的主要降解产物。UCB是一种强效抗氧化分子,也是间接促氧化剂的生成剂。越来越多的证据表明,其主要细胞效应是通过抑制癌细胞系增殖和引发细胞毒性来介导的,尤其是在神经元和神经胶质细胞中。在此,我们描述了一些研究,这些研究表明氧化还原状态的改变和氧化应激的产生可能是UCB诱导细胞毒性的早期事件。然后,我们阐明了一些控制这些效应的分子途径。

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