Arsenic toxicity: Sources, pathophysiology and mechanism Original paper

What was studied?

This review explores the toxicity of arsenic, a naturally occurring element, and its widespread impact on human health. The paper focuses on arsenic exposure, its chemical forms (primarily inorganic arsenite [As3+] and arsenate [As5+]), and how it contributes to various chronic diseases. Arsenic’s toxicity is linked to its interactions with sulfur-containing proteins, and the review examines the significant role of oxidative stress, genotoxicity, and epigenetic changes in arsenic-induced pathogenesis. The review also covers arsenic’s effects on vital organs such as the liver, kidneys, and nervous system, and it discusses potential molecular mechanisms contributing to its toxicity, including mitochondrial dysfunction and signaling pathway disruptions.

Who was studied?

The review includes studies from a range of populations, with a primary focus on those exposed to arsenic through drinking water and environmental sources. Populations in areas with high arsenic levels in groundwater, such as parts of India, Bangladesh, China, and Central and South America, are particularly vulnerable. The paper draws on a wide variety of research, including epidemiological studies, animal models, and laboratory experiments, to illustrate how arsenic exposure leads to different health outcomes across diverse regions and environments. Special emphasis is placed on the effect of arsenic on vulnerable groups, such as children and pregnant women, as well as the potential transgenerational impacts of exposure.

Most important findings

The review highlights arsenic’s extensive impact on human health, particularly its association with chronic diseases such as cancer, cardiovascular disorders, neurotoxicity, and diabetes. Arsenic exposure induces oxidative stress, resulting in the generation of reactive oxygen species (ROS) and mitochondrial dysfunction, which in turn contribute to cellular damage and organ toxicity. The review also emphasizes the role of epigenetic modifications, including histone alterations and changes in DNA methylation, which may affect gene expression and contribute to the long-term health effects of arsenic exposure. Arsenic-induced inflammation and its effects on cellular signaling pathways, such as the NF-κB pathway, were identified as key contributors to its toxic effects. Additionally, the review outlines the carcinogenic effects of arsenic on multiple organs, including the lungs, liver, kidneys, and skin, and underscores the importance of addressing arsenic contamination, especially in regions where exposure remains high.

Key implications

The findings of this review have significant implications for public health and environmental policy. Understanding the complex mechanisms through which arsenic exerts its toxic effects is crucial for developing strategies to mitigate exposure and prevent the associated health risks. The review stresses the need for continued research to fill gaps in our understanding of arsenic toxicity, particularly in terms of the epigenetic changes it induces and its long-term impacts on human health. The review also calls for stronger regulation of arsenic levels in drinking water and for the development of more effective bioremediation and pharmacological approaches to reduce arsenic toxicity. Further studies are necessary to explore the development of therapeutic agents that target specific molecular pathways disrupted by arsenic exposure, as well as interventions that can reduce its impact on vulnerable populations.