Acrylamide-Induced Hepatotoxicity Through Oxidative Stress: Mechanisms and Interventions

Abstract

Significance: Acrylamide (AA) widely exists in the environment. Studies have demonstrated that AA has neurotoxicity and potential carcinogenicity in humans, and genotoxicity and severe hepatotoxicity in animals. As the critical metabolism organ for AA, the liver is the primary attacking target of AA. This review summarizes the recent advances in hepatotoxicity mechanism through AA-induced oxidative stress in rodent livers and hepatic cell lines, this is beneficial to assess risks of AA exposure and explore effective intervention methods for AA hepatotoxicity. Recent Advances: Accumulating evidences have indicated that AA-induced oxidative stress is responsible for its hepatotoxicity. The changes in homological and biochemical indexes such as activities of hepatic antioxidant enzymes have been elucidated with the occurrence and development of oxidative stress. Also, the molecular mechanisms underlying AA-induced hepatotoxicity through oxidative stress have been mainly explained by apoptosis, inflammatory and autophagic pathways. Critical Issues: This review is focusing on the molecular mechanism of hepatotoxicity through AA-induced oxidative stress, this can provide a theoretical basis for the assessment of AA-induced health risk and finding potential intervention targets. Future Directions: Epigenetic modifications like miRNAs and modulation of the gut microbiome involved in AA toxification pathway must be investigated, and will provide novel insights to unravel the toxification mechanism and intervention strategy for AA hepatotoxicity.