Selenium and anticarcinogenesis: underlying mechanisms
Selenium and anticarcinogenesis: underlying mechanisms
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DOI：
10.1097/mco.0b013e3283139674
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发表时间：
2008-11-01
影响因子：
3.1
通讯作者：
Combs, Gerald F., Jr.
中科院分区：
文献类型：
--
作者：
Jackson, Matthew I.;Combs, Gerald F., Jr.
综述的目的讨论最近的研究有关抗癌机制的硒行动的基础化学/生物化学功能的硒物种，可能是这些effectors.Recent findingsRecent研究在各种模型系统增加了认识抗癌机制的硒化合物。这些包括对基因表达、DNA损伤和修复、信号传导途径、细胞周期和凋亡的调节、转移和血管生成的影响。这些效应似乎与氧化还原循环、蛋白质巯基修饰和蛋氨酸模拟产生的活性氧有关。三种主要的硒代谢物似乎执行这些效果：硒化氢，甲基硒醇和硒代甲硫氨酸。各种硒化合物可以代谢为这些物种中的一种或多种，但抗癌活性不同的事实表明它们的代谢和化学/生物化学处置的竞争途径。越来越多的知识硒蛋白多态性已表明，至少有一些与癌症的风险，并可能影响致癌间接影响硒metabolic.SummaryThe抗癌作用的硒化合物构成中间机制与几个潜在的化学/生化机制，如氧化还原循环，改变蛋白质巯基氧化还原状态和蛋氨酸模仿。
Purpose of reviewTo discuss recent research related to anticarcinogenic mechanisms of selenium action in light of the underlying chemical/biochemical functions of the selenium species, likely to be executors of those effects.Recent findingsRecent studies in a variety of model systems have increased the understanding of the anticarcinogenic mechanisms of selenium compounds. These include effects on gene expression, DNA damage and repair, signaling pathways, regulation of cell cycle and apoptosis, metastasis and angiogenesis. These effects would appear to be related to the production of reactive oxygen species produced by the redox cycling, modification of protein-thiols and methionine mimicry. Three principle selenium metabolites appear to execute these effects: hydrogen selenide, methylselenol and selenomethionine. The fact that various selenium compounds can be metabolized to one or more of these species but differ in anticarcinogenic activity indicates competing pathways of their metabolic and chemical/biochemical disposition. Increasing knowledge of selenoprotein polymorphisms has shown that at least some are related to cancer risk and may affect carcinogenesis indirectly by influencing selenium metabolism.SummaryThe anticarcinogenic effects of selenium compounds constitute intermediate mechanisms with several underlying chemical/biochemical mechanisms such as redox cycling, alteration of protein-thiol redox status and methionine mimicry.