Redox state, oxidative stress, and molecular mechanisms of protective and toxic effects of bilirubin on cells.
Redox state, oxidative stress, and molecular mechanisms of protective and toxic effects of bilirubin on cells.
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DOI：
10.2174/138161209789058174
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发表时间：
2009-08
影响因子：
3.1
通讯作者：
G. Tell;S. Gustincich
中科院分区：
文献类型：
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作者：
G. Tell;S. Gustincich
未结合胆红素（UCB）是血红素催化剂的主要降解产物。UCB是一种有效的抗氧化分子，也是一种间接的促氧化剂产生剂。越来越多的证据表明，其主要的细胞效应是通过抑制癌细胞系的增殖和引起细胞毒性，特别是在神经元和神经胶质细胞中介导的。在这里，我们描述的研究表明，氧化还原状态的改变和氧化应激的产生可能是早期事件负责脐血诱导的细胞毒性。然后，我们阐明了一些控制这些影响的分子途径。
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.