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肠道微生物对砷生物转化及多器官毒性影响的研究进展
Research Progress on the Impact of Gut Microbiota on Arsenic Biotransformation and Multiorgan Toxicity

DOI: 10.12677/amb.2025.144019, PP. 156-170

Keywords: 砷,肠道微生物,砷的生物转化,多器官毒效应
Arsenic
, Gut Microbes, Biotransformation of Arsenic, Multi-Organ Toxic Effects

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Abstract:

砷作为一种广泛存在的环境类金属污染物,其慢性暴露可引发心血管疾病、肝癌、糖尿病及神经退行性疾病等多系统病变,已成为全球重大公共卫生挑战。肠道菌群作为连接砷暴露与宿主健康的关键中介,通过“砷–菌群–宿主”轴参与砷的生物转化与毒性调控,其作用机制涉及双向互作:一方面,肠道菌群通过还原、甲基化等代谢过程改变砷的化学形态与毒性;另一方面,砷暴露可诱导肠道菌群多样性降低、结构失衡及屏障功能损伤,进而通过炎症反应、氧化应激、代谢产物紊乱及肠–脑轴等途径,加剧砷诱导的多器官损伤。本文系统综述了砷的代谢特征与多器官毒效应,重点解析了砷暴露对肠道菌群的影响以及肠道菌群在砷生物转化过程中的作用,并阐述了菌群失调与砷相关疾病的关联。本文旨在为理解“砷–菌群–宿主”的作用机制提供全景视角,为开发靶向肠道菌群的砷毒性干预策略及相关疾病防治提供理论依据与潜在靶点。
As a widely existing environmental metalloid pollutant, arsenic can induce multisystem disorders such as cardiovascular diseases, liver cancer, diabetes mellitus, and neurodegenerative diseases upon chronic exposure. This has become a major global public health challenge. The gut microbiota serves as a critical intermediary linking arsenic exposure and host health through the “arsenic-microbiota-host” axis, participating in both the biotransformation and toxicity modulation of arsenic. on one hand, gut microbiota metabolize arsenic through reduction, methylation, and other processes, altering its chemical speciation and toxicity; on the other hand, arsenic exposure disrupts the gut microbial community by reducing diversity, altering composition, and impairing barrier function. These changes exacerbate arsenic-induced multi-organ damage via mechanisms such as inflammatory responses, oxidative stress, metabolic disturbances, and gut-brain axis signaling. This review systematically outlines the metabolic characteristics of arsenic and its multi-organ toxicity, with a focus on how arsenic reshapes the gut microbiota and how microbial metabolism influences arsenic biotransformation. Furthermore, it discusses the correlation between dysbiosis and arsenic-related diseases. The objective of this study is to comprehensively understand the underlying mechanisms among arsenic, the microbiota, and the host, thereby offering a theoretical basis and potential strategies for mitigating arsenic toxicity through microbiota-targeted interventions.

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