Abstract：Arsenic, a known poison and human carcinogen, is widely found in nature. Chronic arsenic exposure can cause skin pigment abnormalities, hyperkeratosis and systemic poisoning dominated by skin and visceral tumors, and the mechanism is not well understood so far. The arsenic compound enters the body and undergoes methylation metabolism. The methyl donor S-adenosyl methionine (SAM) of arsenic methylation process is derived from a carbon unit centered on tetrahydrofolate, and the metabolic loop is regulated by a variety of enzymes. Single nucleotide polymorphisms of these enzymes may indirectly cause differences in methylation metabolism in individuals due to the effects of SAM supply. This review focuses on the functions of key enzymes in a single carbon metabolism loop, genetic polymorphisms and their association with arsenic metabolism and the risk of arsenic poisoning.
杨舒伊, 郎虹, 陈峣, 李昕. 一碳单位酶基因单核苷酸多态对砷代谢及中毒的影响[J]. 实用预防医学, 2019, 26(5): 638-640.
YANG Shu-yi, LANG Hong, CHEN Yao, LI Xin. Effect of single nucleotide polymorphisms of one-carbon unitenzyme gene on arsenic metabolism and poisoning. , 2019, 26(5): 638-640.
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