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Ferroptosis Induced by Micro/Nanoplastics: Mechanisms, Toxic Effects, and Implications for Aquaculture
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This review summarizes existing research on how tiny plastic particles (microplastics and nanoplastics) can trigger a type of cell death called ferroptosis in farmed aquatic animals, damaging organs like the intestine, liver, and gills. It describes the biological mechanisms involved and discusses possible monitoring markers and management approaches for aquaculture settings.
ABSTRACT In aquaculture ecosystems, the accumulation of microplastics and nanoplastics (MNPs) poses an increasing threat to the health, disease resistance, and productivity of farmed species. Ferroptosis, an iron‐dependent cell death driven by lipid peroxidation, offers a new perspective for elucidating the toxicity mechanisms of MNPs. Understanding this mechanism is particularly critical for assessing and mitigating the health risks of MNPs in aquaculture. This paper provides a critical review of recent progress on MNPs‐induced ferroptosis. Mechanistically, MNPs trigger ferroptosis by inducing oxidative stress and lipid peroxidation, disrupting iron homeostasis, inhibiting the GPX4 antioxidant system, and regulating signaling pathways such as Nrf2 and p53/Fosl1. Nanoscale particles may act primarily via endocytosis and intracellular interactions to induce ferroptosis, whereas microscale particles exert effects mainly through surface interactions, mechanical stress, and metabolic disruption, yet the outcome is also modulated by polymer type, surface charge, shape, aging, and protein corona formation. At the organ level, MNPs‐induced ferroptosis is associated with damage to the intestine, gonads, liver, cardiovascular system, nervous system, gills, and immune organs, and is amplified by co‐exposure with heavy metals and organic pollutants. For aquaculture practice, molecular markers such as MDA, GSH, and GPX4 can serve as tiered early warning indicators, with intensive pond and cage culture systems facing the highest risk. Feasible interventions include dietary antioxidant supplementation, water treatment, feed quality control, and regular replacement of aged plastic infrastructure. This review provides a theoretical basis for assessing MNPs health risks and developing practical management strategies for sustainable aquaculture.
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Researchers exposed carp to polyethylene microplastics and found they caused serious intestinal damage through two harmful pathways: ferroptosis (a type of iron-dependent cell death) and NF-kB-driven inflammation. The microplastics triggered a buildup of iron and reactive oxygen species in gut tissue, leading to cell death and tissue destruction. Since humans also ingest microplastics that reach the gut, these findings highlight a potential mechanism by which microplastics could damage our digestive system.
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This review explores the emerging connection between microplastics combined with heavy metals and a type of cell death called ferroptosis, which involves iron-dependent damage to cell membranes. Researchers found that both microplastics and heavy metals can independently trigger ferroptosis, and their combined presence may amplify this effect in organs like the liver, kidneys, and brain. The study suggests that understanding this cell death pathway could provide new insights into how environmental pollutant mixtures contribute to disease.
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