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Polyethylene Microplastics and Cardiometabolic Mitochondrial-Redox Dysfunction in Preclinical Rodent Models: A Systematic Review and Meta-Analysis of Bioenergetic and Oxidative Stress Outcomes Across Target Organs
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This review combined results from 13 rodent studies on polyethylene microplastics. It found that exposure reduced energy-producing enzyme activity and antioxidant levels, while increasing markers of cell damage, across kidney, heart, lung, brain, and reproductive tissues, with the strongest effects seen in heart and lung tissue. Confidence in these findings was rated low to very low.
Polyethylene microplastics (PE-MPs), the most globally abundant plastic polymer, accumulate in rodent tissues following experimental exposure and have been implicated in multi-organ biochemical disruption. Whether mitochondrial bioenergetic failure and redox collapse represent a convergent, organ-transcendent mechanism of PE-MP toxicity has not been quantitatively established. We conducted a PRISMA 2020-guided systematic review and random-effects meta-analysis, searching four electronic databases for controlled rodent studies reporting oxidative phosphorylation enzyme activities and redox markers following PE-MP exposure. Risk of bias was evaluated with SYRCLE, and evidence certainty was graded using a preclinical adaptation of GRADE. Thirteen studies (160 experimental arms, seven organ systems) met inclusion criteria; four studies across five organs supplied quantitative TCA cycle and electron transport chain data for the primary analysis, while the remaining nine contributed redox biomarker data. PE-MPs produced large, significant suppression of all four TCA cycle enzymes (CS: g = -2.69 to -3.82; p ≤ 0.009) and electron transport chain Complexes I, III, and IV (g = -3.08 to -3.70; p < 0.0001); Complex II showed non-significant, organ-specific adaptive upregulation. Pro-oxidant markers MDA and NO rose significantly, with NO showing near-perfect cross-organ homogeneity (I2 = 4.5%). Antioxidants GSH, SOD, and CAT were markedly depleted (g = -2.48, -2.93, -3.86; p < 0.0001). After mandatory GRADE/OHAT downgrades for unclear allocation concealment and single-group data dominance, certainty was Low for ten outcomes and Very Low for six. PE-MPs elicits the potency of being a mitochondrial toxicant via coherent tripartite axis throttling of TCA cycle, electron-leak amplification of the electron transport chain, and peroxynitrite-driven antioxidant exhaustion converging across renal, cardiac, pulmonary, neural, and gonadal tissues, with cardiac and cardiopulmonary mitochondrial injury emerging as a particularly consequential. These findings establish the mitochondrial-redox axis as a defining biochemical fingerprint of PE-MP multi-organ toxicity and provide mechanistic grounding for microplastic-associated cardiovascular risk.
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