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Copyright of Geology & Exploration is the property of Geology & Exploration Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

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铜离子转运蛋白 (CTR) 是一系列参与机体铜离子吸收、转运、利用、贮存和清除等铜 离子稳态调控的复杂体系，在铜离子参与调控氧化应激、能量产生、黑色素形成、神经肽生物发生和 结缔组织成熟等过程中发挥重要作用。电离辐射诱导 CTR 表达的改变影响了铜离子在细胞中的分布， 电离辐射诱导的细胞和组织中铜离子积聚伴有高亲和力铜离子转运蛋白 1 (CTR1) 表达水平明显升高 以及铜外排转运蛋白铜离子转运 ATP 酶 α 肽 (ATP7A) 表达水平降低，进而激活胞内氧化还原反应， 加重正常组织的辐射损伤。铜死亡是一种新的细胞死亡方式，目前已成为研究热点，CTR 可促进电离 辐射后铜死亡的发生，推测辐射引起 CTR1 表达上调和 ATP7A 降解进而导致细胞辐射敏感性增加可 能通过铜死亡途径介导，提示放射损伤的发生发展与 CTR 介导的铜离子稳态调控有密切关联。现对 几种关键铜稳态蛋白及其之间的相互作用、CTR 介导的铜离子稳态调控在正常组织辐射损伤中发挥的 生物学作用和调控机制及与铜死亡的关系进行全面综述，为正常组织辐射损伤的治疗提供新策略。 [ABSTRACT FROM AUTHOR]

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