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Oxidative Stress, Environmental Pollutants, Aging, and Epigenetic Regulation: Mechanistic Insights and Biomarker Advances
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Researchers synthesized 2020–2025 evidence on how environmental pollutants including micro- and nanoplastics amplify reactive oxygen species through shared nodes — mitochondrial disruption, NADPH oxidase activation, and Fenton chemistry — propagating oxidative signals into epigenetic remodeling, while comparing biomarker platforms by analytical specificity and translational readiness.
Environmental pollutants, lifestyle factors, and intrinsic metabolism can amplify reactive oxygen and nitrogen species (ROS/RNS) generation beyond antioxidant capacity. The resulting oxidative stress damages macromolecules, perturbs redox signaling, and may accelerate biological aging. This review synthesizes evidence published mainly in 2020-2025 on how major pollutant classes (air pollutants, metals, pesticides, nanoparticles, and micro-/nanoplastics) induce ROS through shared nodes mitochondrial electron transport disruption, NADPH oxidase activation, and redox cycling/Fenton chemistry and how these signals propagate to epigenetic remodeling (DNA methylation, histone modifications, and non-coding RNAs). To move beyond descriptive cataloging, we grade the strength of evidence by study context (cell culture, animal models, human observational studies, and clinically oriented biomarker research), highlight convergent findings and unresolved controversies, and specify key methodological limits. We then compare oxidative-stress biomarker platforms by analytical specificity, pre-analytical susceptibility, and translational readiness, distinguishing validated markers from exploratory redox-epigenetic and multi-omics signatures. Finally, we discuss how exposomics and AI-assisted multi-omics integration may support biomarker discovery while emphasizing current constraints (confounding, batch effects, and limited prospective validation) that must be addressed for clinical translation.
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