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Hepatic Mitochondrial Dysfunction and Gut Dysbiosis Induced by Polyethylene Microplastics in FVB/n Mice: A Comparative Study of Fluorescent and Non-Fluorescent Particles
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Researchers exposed mice to environmentally representative concentrations of fluorescent and non-fluorescent polyethylene microplastics and found both types disrupted hepatic mitochondrial respiration and altered gut microbiome composition, with fluorescent particles causing more severe mitochondrial damage — highlighting that fluorescent labeling used in many laboratory studies may systematically overestimate toxicity compared to real-world MPs.
The emerging problem that microplastics pose to our society is reflected in the exponential growth in investigations devoted to uncovering their toxicological potential in humans. However, these studies present several limitations, one of the most significant being the use of microplastics that do not represent their environmental counterparts. In this study, we evaluated the impact of two types of polyethylene microplastics (27–32 µm)—non-fluorescent and fluorescent—on the liver and intestine, targeting mitochondria. FVB/n mice were subjected to a subacute exposure to two concentrations representative of human exposure (0.002% (w/w) and 0.006% (w/w)). Both types of microplastics impaired mitochondrial respiration through disruption of NADH-linked pathways, with more pronounced effects at the highest concentration of fluorescent MPs. Electron transport chain complexes, particularly CIII and CIV, were affected, partially explaining the observed alterations in mitochondrial respiratory capacity. An increased SOD and GPx activity supported the link between mitochondrial dysfunction and increased reactive oxygen species overproduction under MPs exposure. Hepatic mitochondrial lipid remodelling was detected following exposure to fluorescent microplastics, while intestinal epithelial cells displayed impaired mitochondrial activity together with compromised cellular integrity, indicative of stress response. In parallel, shifts in gut composition suggest that PE MPs may contribute to intestinal barrier dysfunction. Overall, fluorescent MPs induced more severe mitochondrial and biochemical disturbances in both the liver and the intestine than their non-fluorescent counterparts. Our findings highlight mitochondria as central targets for microplastic-induced toxicity and underscore the need for improved MPs models in toxicological research.
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Comparative Analysis of Metabolic Dysfunctions Associated with Pristine and Aged Polyethylene Microplastic Exposure via the Liver-Gut Axis in Mice
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Mice fed both new and weathered polyethylene microplastics developed disrupted fat metabolism, liver oxidative stress, and shifts in gut bacteria, with weathered (aged) particles causing more severe effects. This study suggests that the microplastics people encounter in the real world, which have been degraded by sunlight and time, may be more harmful than the pristine particles typically used in lab studies.
Comparative Analysisof Metabolic Dysfunctions Associatedwith Pristine and Aged Polyethylene Microplastic Exposure via theLiver-Gut Axis in Mice
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Researchers fed mice low doses of pristine and aged polyethylene microplastics for several weeks and analyzed changes in blood metabolites, liver proteins, and gut bacteria. Both forms caused lipid metabolism disruptions and reduced beneficial gut bacteria, with aged microplastics showing greater toxicity linked to changes in fatty acid processing enzymes.
Renal Mitochondria as Targets of Microplastic Toxicity in Mice: Comparing Fluorescent and Non-Fluorescent Polyethylene Particles
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Scientists fed mice small amounts of microplastic particles for a month and found that the plastic damaged the "power plants" inside kidney cells (mitochondria), reducing their ability to produce energy and triggering cell stress. Interestingly, the glow-in-the-dark plastic particles often used in lab studies caused more damage than plain plastic, suggesting some past microplastic research may not accurately reflect how regular plastic pollution affects our bodies. While this study was in mice, not humans, it adds to growing evidence that ingesting microplastics could harm organ function at the cellular level.
Assessing micro and nanoplastics toxicity using rodent models: Investigating potential mitochondrial implications
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This review examines recent rodent studies investigating how micro- and nanoplastics affect cellular health, with a focus on potential mitochondrial impacts. Researchers found that while no study has directly targeted mitochondrial effects, several reported molecular and biochemical changes consistent with disrupted mitochondrial function, including oxidative stress. The study suggests that mitochondria may be an important but understudied target of micro- and nanoplastic toxicity.
In vivo exposure of mixed microplastic particles in mice and its impacts on the murine gut microbiome and metabolome
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Researchers exposed mice to a mixture of common microplastic types to investigate effects on the gut microbiome and metabolome. The study found that ingested microplastic particles altered gut microbial composition and disrupted metabolic pathways, suggesting that realistic mixed-microplastic exposure may have broader biological effects than single-polymer studies indicate.
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