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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.
Current knowledge on the toxic effects of microplastics (MPs) on human health relies on the extrapolation of data collected from in vivo studies. These studies, however, present limitations, as the particles used often differ from their environmental counterparts. Nevertheless, they provide valuable insights into the mechanisms underlying MPs’ toxicity. In this study, we targeted the mitochondria to investigate the effects of two types of polyethylene microplastics (PE MPs, 27–32 µm), fluorescent and non-fluorescent, on kidneys from FVB/n mice. Animals were exposed for 28 days to two environmentally relevant concentrations of PE MPs (0.002% (w/w) and 0.006% (w/w)). Results reveal that both MPs induce mitochondrial dysfunction, as indicated by oxygen flux depletion in different coupling-controlled states. Complex II dysfunction, particularly at the highest concentration of fluorescent particles, and alterations in other components of the electron transport chain were identified as one of the causes of mitochondrial dysfunction. MPs’ exposure also induced subtle remodelling of the mitochondrial membrane lipid profile, marked by shifts in specific saturated and unsaturated fatty acids, suggesting an adaptive response to preserve membrane integrity. These alterations were accompanied by oxidative stress, evidenced by decreased SOD and CAT activities, particularly under high concentrations of fluorescent PE MPs. Overall, fluorescent MPs triggered stronger mitochondrial and metabolic disruptions in the kidney. All together, these findings reinforce mitochondria as pivotal targets of MPs’ toxicity and highlight the need for improved experimental models that better reflect environmentally relevant exposure scenarios.
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Researchers gave rats polyethylene microplastics orally for 28 days and found dose-dependent kidney damage, including impaired filtration, electrolyte imbalances, and tissue inflammation. The microplastics depleted antioxidant defenses, increased oxidative stress markers, and disrupted mitochondrial energy production in kidney cells, identifying the kidneys as a critical target of microplastic toxicity.
Polystyrene microplastics induce nephrotoxicity through impaired mitochondrial homeostasis: An integrated experimental study
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In an animal study, exposure to polystyrene microplastics built up in the kidneys and caused kidney damage, including harmful oxidative stress, inflammation, and disrupted function of mitochondria, the energy-producing parts of cells. Higher doses caused more buildup and more tissue damage, pointing to the kidney as a key target for microplastic harm.
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.
Impact of Micro- and Nanoplastics on Mitochondria
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This review examines how micro- and nanoplastics can damage mitochondria, the energy-producing structures inside cells that are critical for metabolism and cell survival. Researchers found that plastic particle exposure can trigger oxidative stress, disrupt mitochondrial membrane function, and interfere with energy production pathways. Since mitochondrial dysfunction is linked to numerous health conditions, the study suggests this may be a key mechanism through which plastic pollution affects human health.
Polyethylene Microplastics and Mitochondrial-Redox Dysfunction in Preclinical Rodent Models: A Systematic Review and Meta-Analysis of Bioenergetic and Oxidative Stress Outcomes
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This review pulled together existing animal studies on tiny plastic particles (polyethylene microplastics, common in packaging and everyday products) and found a consistent pattern: these particles seem to damage mitochondria, the "power plants" inside our cells, and trigger harmful oxidative stress, which can wear down tissues over time. Since this research is in rodents, not humans, more studies are needed to confirm the same effects happen in people, but the findings raise real concerns about how the microplastics we're increasingly exposed to might affect long-term cellular health and energy production in our bodies.
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