The blood toll of arsenic: addressing hematological disorders and future directions

Arsenic contamination is a critical global health threat, with the hematological system being a primary target of its toxicity. This review synthesized current scientific literature from PubMed and Web of Science to document arsenic-induced hematotoxicity and evaluate the efficacy of various amelioration strategies. Inorganic arsenic uses a variety of cell membrane transporter proteins, including different proton and phosphate transporters and the anion exchanger Band 3 protein for entry into the cell. Glucose transporters, aquaporins, and ATP-binding cassette transporters are used for the extrusion of arsenic. The markers of hematotoxicity are shown to be severely altered in arsenic-treated fish and mammalian models. Moreover, significant alterations, including DNA methylation, altered T cell populations, increased PBMCs associated with marked neutropenia, apoptosis of blood monocytes, etc., were observed in leucocytes. Transformation of discoidal erythrocytes to echinocytes, followed by spheroechinocytes and eryptosis, is considered an impending cause for arsenic-induced anaemia. Chelating agents, various plant extracts, and/or nutraceutical agents such as ascorbic acid, α-tocopherol, and lipoic acid are found to be protective against arsenic-induced hematotoxicity. This comprehensive documentation offers a clear overview of the research conducted in this vital area, indicating that the management of arsenic-induced hematotoxicity is achievable with the aforementioned compounds or extracts. A comparative analysis using secondary data is essential to ascertain the potency and efficacy of various ameliorative agents. This would provide a complete understanding of hematological arsenicosis and guide future directions for remedial measures.