砷诱导细胞程序性死亡的研究进展  

Progress in arsenic-induced programmed cell death

作　　者：丁思 徐梦柔 梅成镐 杨乾磊 武婧 安艳 Ding Si;Xu Mengrou;Mei Chenghao;Yang Qianlei;Wu Jing;An Yan(Department of Toxicology,School of Public Health,Medical College of Soochow University,Suzhou 215123,China)

机构地区：[1]苏州大学医学部公共卫生学院卫生毒理学系,215123

出　　处：《中华地方病学杂志》2020年第7期542-546,共5页Chinese Journal of Endemiology

基　　金：国家自然科学基金(81811540034、81872646、81573173)。

摘　　要：随着对砷由毒性至药性的"两面性"研究的不断深入,砷通过影响多种细胞程序性死亡(programmed cell death,PCD)引起多器官的损伤受到广泛关注。研究显示,砷在体内代谢过程中产生的活性氧(reactive oxygen species,ROS)与其诱导PCD的发生密切相关,然而其具体分子机制仍不清楚。文中就近年来国内外有关砷通过产生ROS诱导细胞凋亡、自噬和程序性坏死等主要的PCD形式及其可能机制的研究进行综述,为进一步研究和防治砷毒性作用提供基础资料,有助于更好地临床开发和利用砷剂治疗肿瘤及相关疾病。With the deepening of the research on the"two sides"of arsenic from poison to medicine,arsenic has attracted extensive attention in affecting programmed cell death(PCD)and causing damage to a variety of organs.Recent studies have showed that reactive oxygen species(ROS)produced by intracellular arsenic metabolism is closely related to PCD induction.However,the specific mechanism is still unclear.In this paper,we have reviewed the main PCD forms,such as apoptosis,autophagy and necroptosis induced by arsenic via ROS and their possible mechanisms,in order to provide basic information for further research and prevention of arsenic toxicity,which is helpful for clinical development and utilization of arsenic in the treatment of tumors and related diseases.

关 键 词：砷 活性氧 程序性死亡 

分 类 号：R994.3[医药卫生—毒理学]