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Differential effects of polyethylene, polystyrene, and polypropylene microplastics on mitochondrial gene expression in tadpoles of Polypedates megacephalus (Anura: Rhacophoridae)
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This study exposed tadpoles of the four-lined tree frog to three types of microplastics and used RT-qPCR to measure mitochondrial gene expression changes after 14 days. The three polymer types produced distinct transcriptional responses: polyethylene upregulated ND4 suggesting compensatory ATP production, polystyrene increased COI linked to redox effects, and polypropylene downregulated ND4L and ND6 indicating reactive oxygen species-mediated mitochondrial complex I dysfunction.
As emerging pollutants, microplastics accumulate in aquatic environments through diverse transport mechanisms, posing global ecological threats. This study investigated mitochondrial gene expression responses in Polypedates megacephalus tadpoles exposed to 60 mg/L of 5 μm polyethylene (PE), polystyrene (PS), and polypropylene (PP) microplastics for 14 days using real-time quantitative polymerase chain reaction (RT-qPCR) (P < 0.05). The results revealed distinct polymer-specific transcriptional patterns. PE exposure significantly upregulated ND4 expression to 2.224 ± 0.216-fold relative to the control (set as 1.0), suggesting a compensatory increase in ATP production through enhanced proton pumping. PS increased COI transcript levels to 1.638 ± 0.262-fold, which may be associated with modulation of redox homeostasis under conditions of disrupted lipid metabolism. In contrast, PP exposure markedly downregulated ND4L and ND6 expression to 54.5% (0.545 ± 0.088) and 27.2% (0.272 ± 0.093) of control levels, respectively. These alterations indicate Reactive Oxygen Species (ROS)-mediated dysfunction of mitochondrial complex I. In conclusion, the three microplastics induce the specific expression of mitochondrial genes through differentiated molecular mechanisms, providing a new perspective for understanding polymer-dependent toxicity. This study reveals the molecular interference pathways of microplastics on aquatic organisms and highlights the core role of mitochondrial function in the stress response to pollutants.
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