Polystyrene microplastics-induced cardiotoxicity in chickens via the ROS-driven NF-κB-NLRP3-GSDMD and AMPK-PGC-1α axes

Microplastics (MPs) pollution is getting increasingly prominent, and its dangers have attracted widespread attention. The heart is the central hub of the organism's survival, and the mechanism of MPs-induced heart injury in chickens is unknown. Here, we investigated the effects of 5 μm polystyr...

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Veröffentlicht in:The Science of the total environment 2022-09, Vol.840, p.156727-156727, Article 156727
Hauptverfasser: Zhang, Yue, Yin, Kai, Wang, Dongxu, Wang, Yu, Lu, Hongmin, Zhao, Hongjing, Xing, Mingwei
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Sprache:eng
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Zusammenfassung:Microplastics (MPs) pollution is getting increasingly prominent, and its dangers have attracted widespread attention. The heart is the central hub of the organism's survival, and the mechanism of MPs-induced heart injury in chickens is unknown. Here, we investigated the effects of 5 μm polystyrene microplastics (PS-MPs) on the heart and primary cardiomyocytes of chickens at varied concentrations. We observed that PS-MPs caused severe pathological damage and ultrastructural changes in heart, induced myocardial pyroptosis, inflammatory cell infiltration and mitochondrial lesions. PS-MPs evoked abnormal antioxidant enzyme content and ROS overproduction. Detailed mechanistic investigation indicated that PS-MPs triggered pyroptosis via NF-κB-NLRP3-GSDMD axis and exacerbated myocardial inflammation (NLRP3, Caspase-1, IL-1β, IL-18, ASC, GSDMD, NF-κB, COX-2, iNOS and IL-6 overexpression). Additionally, PS-MPs induced mitochondrial damage (TFAM, OPA1, MFN1 and MFN2 down-expression, DRP1 and Fis1 overexpression) and energy metabolism disorders (HK2, PKM2, PDHX and LDH up-regulation) by inhibiting AMPK-PGC-1α pathway. Interestingly, NAC alleviated these aberrant manifestations in vitro. We suggested that PS-MPs driven alterations in NF-κB-NLRP3-GSDMD and AMPK-PGC-1α pathways via ROS overload, which in turn triggered oxidative stress, myocardial pyroptosis, inflammation, mitochondrial and energy metabolism dysfunction. This provided theoretical bases for protecting chickens from toxic injury by MPs. [Display omitted] •PS-MPs exposure triggered oxidative stress and ROS overload in myocardium.•PS-MPs induced cardiac pyroptosis and inflammation by the NF-κB-NLRP3-GSDMD axis.•PS-MPs caused abnormal mitochondrial and energy metabolism by the AMPK-PGC-1α axis.•PS-MPs elicited cardiotoxicity in chickens may depend on the driving effect of ROS.
ISSN:0048-9697
1879-1026
DOI:10.1016/j.scitotenv.2022.156727