Rikiishi Hidemi
Department of Microbiology and Immunology, Tohoku University Graduate School of Dentistry, 4-1 Seiryo-machi, Sendai 980-8575, Japan.
J Bioenerg Biomembr. 2007 Feb;39(1):91-8. doi: 10.1007/s10863-006-9065-7.
Converging data from epidemiological, ecological, and clinical studies have shown that selenium (Se) can decrease the risk for some types of human cancers. Induction of apoptosis is considered an important cellular event that can account for the cancer preventive effects of Se. Prior to occurrence of apoptosis, Se compounds alter the expression and/or activities of signaling molecules, mitochondria-associated factors, transcriptional factors, tumor suppressor genes, and cellular reduced glutathione. Mechanistic studies have demonstrated that the methylselenol metabolite pool has many desirable attributes of chemoprevention, whereas the hydrogen selenide pool with excess of selenoprotein synthesis can lead to DNA single-strand breaks. To elucidate the effects of Se on cytotoxic events, it should be remembered that the chemical forms and the dose of Se, and the experimental system used, are determinants of its biological activities. This mini-review focuses on elucidation of the molecular mechanisms of cancer prevention by Se with the apoptotic approach.
来自流行病学、生态学和临床研究的汇聚数据表明,硒(Se)可降低某些类型人类癌症的风险。细胞凋亡的诱导被认为是一个重要的细胞事件,它可以解释硒的癌症预防作用。在细胞凋亡发生之前,硒化合物会改变信号分子、线粒体相关因子、转录因子、肿瘤抑制基因和细胞内还原型谷胱甘肽的表达和/或活性。机制研究表明,甲基硒醇代谢物库具有许多理想的化学预防特性,而过量合成硒蛋白的硒化氢库可导致DNA单链断裂。为了阐明硒对细胞毒性事件的影响,应该记住,硒的化学形式和剂量以及所使用的实验系统是其生物活性的决定因素。本综述聚焦于用细胞凋亡方法阐明硒预防癌症的分子机制。