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Polyethylene microplastics induced inflammation via the miR-21/IRAK4/NF-κB axis resulting to endoplasmic reticulum stress and apoptosis in muscle of carp
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Researchers found that polyethylene microplastics caused muscle damage in carp through a specific chain reaction: the plastics reduced a protective molecule called miR-21, which activated an inflammatory pathway (NF-kB), leading to stress in the cell's protein-folding machinery and ultimately cell death. This molecular-level finding helps explain how microplastics could damage muscle tissue in fish, with potential implications for the safety of fish consumed by humans.
As a widespread environmental pollutant, microplastics pose a great threat to the tissues and organs of aquatic animals. The carp's muscles are necessary for movement and survival. However, the mechanism of injury of polyethylene microplastics (PE-MPs) to carp muscle remains unclear. Therefore, in this study, PE-MPs with the diameter of 8 μm and the concentration of 1000 ng/L were used to feed carp for 21 days, and polyethylene microplastic treatment groups was established. The results showed that PE-MPs could cause structural abnormalities and disarrangement of muscle fibers, and aggravate oxidative stress in muscles. Exposure to PE-MPs reduced microRNA (miR-21) in muscle tissue, negatively regulated Interleukin-1 Receptor Associated Kinase 4 (IRAK4), activated Nuclear Factor Kappa-B (NF-κB) pathway, induced inflammation, and led to endoplasmic reticulum stress and apoptosis. The present study provides different targets for the prevention of muscle injury induced by polyethylene microplastics.
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Researchers exposed carp to polystyrene microplastics and found they caused heart tissue inflammation, cell death, and necrosis through activation of the TLR4/NF-kB inflammatory pathway. The damage increased with higher microplastic concentrations, with both apoptosis and necrosis observed in heart muscle cells. The study provides evidence that microplastic exposure can directly harm cardiovascular tissue in fish.
Polyethylene microplastics cause apoptosis via the MiR-132/CAPN axis and inflammation in carp ovarian
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Researchers exposed carp to polyethylene microplastics in water and found that the particles caused significant damage to the fish's ovarian tissue through both cell death and inflammation. They identified a specific molecular pathway involving a microRNA and a protein-cutting enzyme that mediated the harmful effects on reproductive cells. The study provides evidence that microplastic contamination in waterways could impair the reproductive health of commonly consumed fish species.
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Researchers fed carp water containing polystyrene microplastics and found significant liver damage, including inflammation, disrupted cell recycling processes, and cell death. The microplastics triggered a stress response in the cell's protein-folding machinery (endoplasmic reticulum), which set off a chain reaction of inflammation and tissue damage. These findings in freshwater fish suggest that microplastics can cause serious organ damage through specific cellular stress pathways.
Polyethylene microplastics trigger cell apoptosis and inflammation via inducing oxidative stress and activation of the NLRP3 inflammasome in carp gills
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Researchers exposed carp gills to polyethylene microplastics and found that the particles triggered cell death and inflammation through oxidative stress and activation of a key immune signaling pathway called the NLRP3 inflammasome. Higher microplastic concentrations caused more severe gill tissue damage and stronger inflammatory responses. The study reveals a specific molecular mechanism by which microplastics can harm the immune function of freshwater fish.
Polystyrene microplastics induce endoplasmic reticulum stress, apoptosis and inflammation by disrupting the gut microbiota in carp intestines
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Researchers fed carp polystyrene microplastics and found that the particles disrupted their gut bacteria, killing off beneficial species and promoting those linked to diseases. The microplastics triggered a stress response in intestinal cells that led to inflammation, cell death, and tissue damage. Since carp is a widely eaten fish, these gut health effects raise questions about how microplastics in aquatic environments could affect the safety of fish that humans consume.
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