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Polystyrene microplastics induce myocardial inflammation and cell death via the TLR4/NF-κB pathway in carp

Fish & Shellfish Immunology 2023 59 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 60 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Kan Li, Qirui Zhang, Fuhan Wang, Jie Cui, Jie Cui, Fuhan Wang, Fuhan Wang, Shuang Xu, Fuhan Wang, Fuhan Wang, Fuhan Wang, Qirui Zhang, Fuhan Wang, Fuhan Wang, Jie Cui, Qirui Zhang, Kan Li, Shuang Xu, Jie Cui, Fuhan Wang, Shuang Xu, Fuhan Wang, Shiwen Xu Shiwen Xu Shiwen Xu Shiwen Xu Qirui Zhang, Shuang Xu, Jie Cui, Shiwen Xu Mengyao Guo, Shiwen Xu Shiwen Xu Shiwen Xu Mengyao Guo, Shiwen Xu Jie Cui, Mengyao Guo, Mengyao Guo, Shiwen Xu Mengyao Guo, Shiwen Xu Shiwen Xu Mengyao Guo, Kan Li, Mengyao Guo, Mengyao Guo, Shiwen Xu Shiwen Xu Shiwen Xu Shiwen Xu Shiwen Xu Mengyao Guo, Shiwen Xu Mengyao Guo, Mengyao Guo, Mengyao Guo, Shiwen Xu Shiwen Xu Mengyao Guo, Kan Li, Shiwen Xu Shiwen Xu

Summary

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.

Polymers
Body Systems

Microplastics (MPs) have attracted widespread attention as an emerging environmental pollutant. Especially in aquatic ecosystems, the harm of MPs to aquatic animals has increasingly become a severe environmental problem. In this study, we constructed a carp polystyrene microplastics (PS-MPs) exposure model to explore the damage and mechanism of PS-MPs exposure to carp myocardial tissue. The results of H&E, TUNEL, and AO/EB staining showed that PS-MPs exposure could induce inflammation, apoptosis, and necrosis in carp myocardial tissue and cardiomyocytes. In addition, our study explored the targeting relationship between PS-MPs and TLR4 and found that PS-MPs exposure could significantly increase the expression of TLR4 pathway-related factors. As the concentration of PS-MPs increased, the NF-κB pathway and inflammation-related factors increased dose-dependent. In addition, myocardial injury induced by exposure to PS-MPs was predominantly apoptotic, accompanied by necrosis. In short, our data suggest that PS-MPs cause damage to myocardial tissue via the TLR4\NF-κB pathway. The above findings enrich the theory of toxicological studies on PS-MPs and provide an essential reference for aquaculture.

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