Mitochondrial Dysfunction in Arsenic-Induced Hepatotoxicity: Pathogenic and Therapeutic Implications

Mitochondria are vital cellular organelles associated with energy production as well as cell signaling pathways. These organelles, responsible for metabolism, are highly abundant in hepatocytes that make them key players in hepatotoxicity. The literature suggests that mitochondria are targeted by various environmental pollutants. Arsenic, a toxic metalloid known as an environmental pollutant, readily contaminates drinking water and exerts toxic effects. It is toxic to various cellular organs; among them, the liver seems to be most affected. A growing body of evidence suggests that within cells, arsenic is highly toxic to mitochondria and reported to cause oxidative stress and alter an array of signaling pathways and functions. Hence, it is imperative to highlight the mechanisms associated with altered mitochondrial functions and integrity in arsenic-induced liver toxicity. This review provides the details of mechanistic aspects of mitochondrial dysfunction in arsenic-induced hepatotoxicity as well as various ameliorative measures undertaken concerning mitochondrial functions.

Automated summary

Mitochondria, as essential cellular organelles associated with energy production and signaling pathways, are targeted by environmental pollutants such as arsenic. Arsenic, a toxic metalloid contaminant of drinking water, is particularly toxic to cellular organs like the liver, primarily affecting mitochondrial function and integrity. Research suggests that arsenic induces oxidative stress and alters signaling pathways within cells, emphasizing the importance of understanding mechanistic aspects of mitochondrial dysfunction in arsenic-induced hepatotoxicity.