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Potential toxicity of microplastics on vertebrate liver: A systematic review and meta–analysis
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This meta-analysis of 118 studies found that microplastics damage vertebrate livers by inducing oxidative stress and intracellular toxicity, altering biotransformation processes, and disrupting lipid metabolism. Organisms at earlier life stages, exposed to smaller particles, and for longer durations showed the greatest liver damage, with catalase, GST, reactive oxygen species, and alkaline phosphatase levels progressively increasing with microplastic concentration.
Microplastics (MPs) pollution is emerging as a significant environmental concern, threatening human and animal health. Liver, as an important organ, plays an important role in the metabolism and detoxification of pollutants. Many studies have suggested that the liver is a potential target organ for MPs. However, the extent and consequences of the impacts of MPs on the liver reported in studies remain inconsistent. We categorized vertebrates into fish, mammals, and birds and performed a meta-analysis to comprehensively examine the effects of MPs on the liver. Hedges' g values were calculated to evaluate effect sizes. To further explore the sources of heterogeneity among the studies, we conducted subgroup analyses focusing on life stage, MPs type, MPs size, and exposure duration. Additionally, we normalized the MPs concentrations and conducted meta-regression analyses to explore the relationship between MPs concentrations and their hepatotoxic effects. A total of 118 studies were included in this meta-analysis. By quantifying 19 indicators, the results showed that MPs could damage the liver by altering liver morphology, inducing oxidative stress, producing intracellular toxicity, altering biotransformation processes, and disturbing lipid metabolism. Intracellular toxicity, followed by oxidative stress, had the greatest impact. Organisms are more sensitive to MPs under the following conditions: longer exposure duration, smaller MPs sizes, and earlier life stages. As the concentration of MPs increases, the levels of several liver indicators, including catalase, glutathione S-transferase, reactive oxygen species, and alkaline phosphatase, progressively increase. This study provides a comprehensive understanding of the effects of MPs on the liver and suggests the underlying mechanisms of MPs hepatotoxicity.
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This meta-analysis found that microplastic exposure significantly impairs fish liver function, elevating key liver enzymes (AST, ALT, ALP, LDH) and triggering oxidative stress markers in liver tissue. The toxicological mechanisms include inflammation, apoptosis, and metabolic disruption, raising concerns about the health of fish populations in microplastic-contaminated waters and the safety of fish as a human food source.
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This meta-analysis of 70 studies across mice, fish, crabs, and shrimp found that microplastic exposure significantly increases liver enzymes (ALT, AST), oxidative stress marker MDA, and pro-inflammatory cytokines (IL-6, TNF-alpha), while reducing protective antioxidant enzymes (SOD, CAT, GSH, GPx). The findings demonstrate that microplastics disrupt liver function through oxidative stress and inflammation across multiple animal species.
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This review summarizes existing research on how microplastics damage the liver, which is a key organ for filtering toxins from the body. Studies show that microplastics can cause liver tissue damage, trigger cell death, and disrupt fat metabolism, with smaller particles and longer exposure causing worse effects. The findings highlight the liver as a particularly vulnerable organ because it accumulates microplastics that enter the body through food and water.
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