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The emerging role of microplastics in systemic toxicity: Involvement of reactive oxygen species (ROS)
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This review examines how microplastics and nanoplastics cause damage at every level of biological complexity -- from molecules and cells to organs and organ systems -- primarily by generating harmful molecules called reactive oxygen species (ROS). These ROS trigger chain reactions including DNA damage, protein breakdown, and cell death pathways, which may contribute to inflammation and disease in exposed organisms, including humans.
Plastic pollution is one of the most pressing environmental threats the world is facing currently. The degradation of macroplastics into smaller forms viz. microplastics (MPs) or Nanoplastics (NPs) is a potential threat to both terrestrial and marine ecosystems and also to human health by directly affecting the organs and activating a plethora of intracellular signaling, that may lead to cell death. There is accumulating evidence that supports the serious toxicity caused by MP/NPs at all levels of biological complexities (biomolecules, organelles, cells, tissues, organs, and organ systems) and the involvement of the reactive oxygen species (ROS) in this process. Studies indicate that MPs or NPs can accumulate in mitochondria and further disrupt the mitochondrial electron transport chain, cause mitochondrial membrane damage, and perturb the mitochondrial membrane potential or depolarization of the mitochondria. These events eventually lead to the generation of different types of reactive free radicals, which can induce DNA damage, protein oxidation, lipid peroxidation, and compromization of the antioxidant defense pool. Furthermore, MP-induced ROS was found to trigger a plethora of signaling cascades, such as the p53 signaling pathway, Mitogen-activated protein kinases (MAPKs) signaling pathway including the c-Jun N-terminal kinases (JNK), p38 kinase, and extracellular signal related kinases (ERK1/2) signaling cascades, Nuclear factor erythroid 2-related factor 2 (Nrf2)-pathway, Phosphatidylinositol-3-kinases (PI3Ks)/Akt signaling pathway, and Transforming growth factor-beta (TGF-β) pathways, to name a few. As a consequence of oxidative stress caused by the MPs/NPs, different types of organ damage are observed in living species, including humans, such as pulmonary toxicity, cardiotoxicity, neurotoxicity, nephrotoxicity, immunotoxicity, reproductive toxicity, hepatotoxicity, etc. Although presently, a good amount of research is going on to access the detrimental effects of MPs/NPs on human health, there is a lack of proper model systems, multi-omics approaches, interdisciplinary research, and mitigation strategies.
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Microplastic toxicology research has focused primarily on apical endpoints (mortality, growth, reproduction) rather than mechanisms, but this review identifies reactive oxygen species formation as the likely molecular initiating event in adverse outcome pathways, leading to oxidative stress, inflammation, and organ-level damage.
Microplastics and nanoplastics in human toxicity: ROS-mediated mechanisms, cellular damage and systemic effects
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This review pulls together existing research showing how tiny plastic particles (microplastics and nanoplastics) can get inside our cells and trigger a damaging cascade of "oxidative stress", essentially cellular rust that harms our DNA, mitochondria (the cell's energy factories), and other vital structures. This damage has been linked in studies to problems throughout the body, including liver and kidney injury, fertility issues, gut bacteria imbalances, hormone disruption, and increased cancer risk, meaning the plastic exposure we experience daily through food, water, and air may have far-reaching effects on our health.
The reactive oxygen species as pathogenic factors of fragmented microplastics to macrophages
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Researchers tested how fragment-shaped microplastics from polypropylene and polystyrene affect different human cell types and found that immune cells called macrophages were the most vulnerable. The toxicity was driven by the microplastics' ability to generate reactive oxygen species (ROS), and interestingly, weathered plastics were less toxic because environmental aging made them better at binding protective proteins. The study suggests that macrophages are a primary target cell for ingested microplastics and that oxidative stress is a key mechanism of their toxicity.
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This review maps the biological harm caused by micro- and nanoplastics to formal toxicity pathways, finding that oxidative stress is a common starting point for damage at every level from cells to whole organisms. Researchers found that in ecological settings, this oxidative damage cascades into growth inhibition and behavioral changes, while in human health contexts it may trigger inflammatory responses. The study highlights that more mammalian research is needed to fully define the health risks of plastic particle exposure.
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