硒代谢,硒蛋白和癌症预防机制:复杂性和硫氧还蛋白还原酶。
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硒代谢,硒蛋白和癌症预防机制:复杂性和硫氧还蛋白还原酶。
致癌作用。1999年9月,20 (9):1657 - 66。
- PubMed ID
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10469608 (在PubMed]
- 文摘
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许多研究在动物模型和人类最近的研究已经证明癌症chemopreventive影响Se。有大量的证据表明,monomethylated形式的Se Se为chemopreventive代谢物的影响至关重要。在转化细胞诱导凋亡是一个重要的chemopreventive机制。可以引发细胞凋亡水平微摩尔的monomethylated形式的Se独立于DNA损伤和细胞中有一个零p53表型。细胞周期蛋白激酶cdk2和蛋白激酶C是由各种形式的强烈抑制。抑制机制涉及修改的半胱氨酸残基在蛋白质本身提出了涉及selenotrisulfide Se加合物的形成(S-Se-S)或selenenylsulfide (S-Se)类型或催化二硫的形成。硒可能促进蛋白质的半胱氨酸残基的瞬态反应形成更多的活性S-Se中间体。小说chemopreventive机制提出了涉及二硫化硒催化的可逆半胱氨酸/转换发生在许多redox-regulated蛋白质,包括转录因子。有时限的激活机制,这种蛋白质,与失活了,将允许正常化的关键细胞过程的早期阶段转换。存在不确定性,目前关于硒蛋白的作用在化学预防模型系统supranutritional Se的水平在哪里工作。 Mammalian thioredoxin reductase is one selenoprotein that shows increased activity with Se supplementation in the nutritional to supranutritional range. Enhanced thioredoxin reduction could have beneficial effects in oxidative stress, but possible adverse effects are considered. Other functions of thioredoxin reductase may be relevant to cell signaling pathways. The functional status of the thioredoxin/thioredoxin reductase system during in vivo chemoprevention with Se has not been established. Some in vitro studies have shown inhibitory effects of Se on the thioredoxin system correlated with growth inhibition by Se. A potential inactivating mechanism for thioredoxin reductase or other selenoenzymes involving formation of a stable diselenide form resistant to reduction is discussed. New aspects of Se biochemistry and possible functions of new selenoproteins in chemoprevention are described.
