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Exposure to microplastics and liver oncogenesis: A comprehensive review on molecular mechanisms and pathogenic pathways
Summary
Researchers reviewed mechanisms by which microplastic exposure may promote liver cancer, identifying oxidative stress, mitochondrial dysfunction, inflammatory signaling, and epigenetic disruption as key pathways, while noting that microplastics can also carry heavy metals and organic pollutants that synergistically amplify hepatotoxic and carcinogenic risk.
Microplastics have become a serious environmental pollutant that enter different ecosystems and eventually the human body through direct exposure to the environment. This infiltration is a major health risk, especially for the liver, which is a primary metabolic organ highly sensitive to the harmful effects of microplastics. There are many ways that these particles can cause liver damage, such as disrupting metabolism, inducing oxidative stress, causing mitochondrial dysfunction, causing inflammation, changing gene expression, and activating abnormal signaling pathways. Even in the absence of hepatic fibrosis or cirrhosis, the carcinogenic potential of microplastics may exert its effects through different pathways. In addition, microplastics can act as efficient vectors for the transport of heavy metals, organic pollutants, and pathogenic microorganisms, thereby synergistically amplifying the toxic effects of these agents and increasing health risks. The complex interactions between microplastics and various pathological processes underscore their critical role in the development of hepatocellular carcinoma. Future research endeavors should focus on elucidating the long-term health impacts of microplastic exposure to devise effective public health policies and preventive strategies.