硒在细胞死亡中的作用

Pengning Gao, Chuanlin Wang, Jia-Li Xu, Shan-Ling Liu, Lan Zhou
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引用次数: 0

摘要

摘要 硒是一种与体内氧化还原平衡密切相关的必需营养素。氧化还原失衡会对细胞内外的微环境产生不利影响,导致细胞死亡。近年来发现了各种类型的细胞死亡,但硒的作用和相关作用机制还需要进一步阐述。我们回顾了硒在细胞坏死、凋亡、铁凋亡、自噬和热凋亡中的作用和作用机制。在正常情况下,硒通过下调核因子κB通路、上调抗凋亡蛋白、降低氧化应激、提高抗氧化酶活性、增强mTOR通路和下调NLRP3/caspase-1通路来抑制细胞坏死、凋亡、铁凋亡、自噬和热噬,从而帮助维持细胞的正常生理功能。另一方面,缺硒会导致 PI3K/AKT 和 Notch/Hes1 通路被激活,使机体氧化应激水平显著升高,从而导致细胞坏死、凋亡和热解。在恶性肿瘤中,无机硒的体内代谢产物硒化氢因其氧化还原活性高,可诱导肿瘤细胞凋亡和铁跃迁,从而发挥抗肿瘤作用。总之,体内充足的硒对维持正常的细胞生理功能和减少纤维化改变至关重要。此外,无机硒的体内代谢产物可能在抗肿瘤治疗中具有一定的临床价值。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Role of selenium in cell death
Abstract Selenium is an essential nutrient closely related to redox homeostasis in the body. A redox imbalance will adversely affect the microenvironment inside and outside the cell, leading to cell death. Various types of cell death have been discovered in recent years, but the role(s) of selenium and the associated mechanism(s) of action require further elaboration. We review the roles and mechanisms of action of selenium in cell necrosis, apoptosis, ferroptosis, autophagy, and pyroptosis. Under normal conditions, selenium inhibits cell necrosis, apoptosis, ferroptosis, autophagy, and pyroptosis by downregulating the nuclear factor κB pathway, upregulating antiapoptotic proteins, decreasing oxidative stress, increasing antioxidant enzyme activity, enhancing the mTOR pathway, and downregulating the NLRP3/caspase-1 pathway, thereby helping to maintain the normal physiological functions of cells. On the other hand, selenium deficiency leads to activation of the PI3K/AKT and Notch/Hes1 pathways, causing a significant increase in the level of oxidative stress in the organism, resulting in cell necrosis, apoptosis, and pyroptosis. In the case of malignancy, the in vivo metabolite of inorganic selenium, hydrogen selenide, plays an antitumor role by inducing apoptosis and ferroptosis in tumor cells because of its high redox activity. In conclusion, an adequate level of selenium in the body is essential for maintaining normal cellular physiological functions and reducing fibrotic alterations. Furthermore, the in vivo metabolites of inorganic selenium may have some clinical value in antitumor therapy.
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