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Polystyrene microplastics mediate cell cycle arrest, apoptosis, and autophagy in the G2/M phase through ROS in grass carp kidney cells
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Researchers found that polystyrene microplastics cause kidney cell damage in fish by triggering oxidative stress, which leads to cells getting stuck in their growth cycle, programmed cell death, and self-digestion. Higher concentrations of microplastics caused worse damage, with reduced antioxidant defenses and increased harmful cellular responses. While this study used fish cells, the mechanisms of cellular damage are relevant to understanding potential risks in other organisms including humans.
Microplastics (MPs) have attracted widespread worldwide attention as a new pollutant. However, the role of reactive oxygen species (ROS) and cell cycle in nephrotoxicity induced by different concentrations of polystyrene microplastics (PS-MPs) is unknown. This study used grass carp kidney cells (CIK) treated with different concentrations of PS-MPs (0, 0.012, 0.0625, and 0.5 mg L-1 ) as subjects. With the increase of PS-MPs concentration, the levels of ROS and malonaldehyde increased, while the level of total antioxidant capacity, superoxide Dismutase (SOD), and glutathione (GSH) activity decreased. The expression of BUB1 mitotic checkpoint serine/threonine kinase (BUB1), cyclin-dependent kinase (CDK1), CDK2, CyclinB1, cell division cycle 20 homolog (CDC20), and B-cell lymphoma-2, sequestosome 1 decreased significantly. Nevertheless, the expression of Caspase 3, Cleave-Caspase 3, cytochrome c (Cytc), BCL2-associated X, apoptosis regulator, poly ADP-ribose polymerase (PARP), Cleave-PARP, Caspase 9, autophagy immunoblot kit (LC3), and Beclin1 increased. Our research shows that PS-MPs can trigger oxidative stress and induce cell cycle arrest, apoptosis, and autophagy in CIK cells by regulating ROS. This work provides a theoretical basis for cellular biology and toxicology mechanisms and new insights into the potential risks to animals from MPs exposure in the environment.
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The involvement of oxidative stress mediated endoplasmic reticulum pathway in apoptosis of Golden Pompano (Trachinotus blochii) liver under PS-MPs stress
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Researchers exposed golden pompano, a commercially important marine fish in China, to polystyrene microplastics at three concentrations for 14 days and observed slowed growth and significant liver damage. The microplastics induced oxidative stress and triggered endoplasmic reticulum-mediated apoptosis in liver cells. The study provides evidence that coastal aquaculture species face real toxicological risks from microplastic pollution in their farming environments.
Influence of Polystyrene Microplastics on Mitochondrial Oxidative Damage in Renal and Muscular Tissues of the Freshwater Fish
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Researchers exposed freshwater fish to environmentally relevant concentrations of polystyrene microplastics for up to 15 days and examined mitochondrial damage in kidney and muscle tissues. The exposure disrupted antioxidant defenses, increased oxidative stress, and altered metabolic enzyme activities in both tissue types. Histological examination revealed significant tissue damage including necrosis and degeneration, suggesting that microplastics can cause organ-level toxicity in fish through mitochondrial oxidative stress.
Polystyrene microplastics induce apoptosis via ROS-mediated p53 signaling pathway in zebrafish
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Researchers discovered that polystyrene microplastics trigger programmed cell death in zebrafish gills through a molecular pathway involving reactive oxygen species and the p53 gene. The microplastics caused dose- and time-dependent oxidative damage, inflammation, and physical injury to gill tissue at concentrations as low as 10 micrograms per liter. The study provides molecular-level evidence explaining how microplastic exposure can harm aquatic organisms.
Acute In Vitro Effects of Polystyrene Microplastics on Cell Viability, Oxidative Status, and DNA Integrity in Zebrafish Erythrocytes
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Scientists exposed fish blood cells to polystyrene microplastics (a common plastic found in packaging and utensils) in a lab dish and found that within just 30 to 90 minutes, the plastic particles killed cells, damaged their DNA, and triggered harmful oxidative stress. While this study used fish cells rather than human ones, it adds to growing evidence that microplastics—which we regularly ingest and inhale—may pose real risks to our cells' health, making the case for further research on human exposure.
Polystyrene microplastics induce nephrotoxicity through impaired mitochondrial homeostasis: An integrated experimental study
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In an animal study, exposure to polystyrene microplastics built up in the kidneys and caused kidney damage, including harmful oxidative stress, inflammation, and disrupted function of mitochondria, the energy-producing parts of cells. Higher doses caused more buildup and more tissue damage, pointing to the kidney as a key target for microplastic harm.
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