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Renal Mitochondria as Targets of Microplastic Toxicity in Mice: Comparing Fluorescent and Non-Fluorescent Polyethylene Particles
Summary
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.