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Polystyrene nanoplastics and cadmium co-exposure aggravated cardiomyocyte damage in mice by regulating PANoptosis pathway
Environmental Pollution ( IF 7.6 ) Pub Date : 2024-03-08 , DOI: 10.1016/j.envpol.2024.123713
Jiali Ye 1 , Wenyue Qiu 1 , Xiaoyue Pang 1 , Yiman Su 1 , Xinting Zhang 1 , Jianjia Huang 1 , Haoming Xie 1 , Jianzhao Liao 1 , Zhaoxin Tang 1 , Zefeng Chen 2 , Fei Li 2 , Zhaojun Xiong 2 , Rongsheng Su 1
Environmental Pollution ( IF 7.6 ) Pub Date : 2024-03-08 , DOI: 10.1016/j.envpol.2024.123713
Jiali Ye 1 , Wenyue Qiu 1 , Xiaoyue Pang 1 , Yiman Su 1 , Xinting Zhang 1 , Jianjia Huang 1 , Haoming Xie 1 , Jianzhao Liao 1 , Zhaoxin Tang 1 , Zefeng Chen 2 , Fei Li 2 , Zhaojun Xiong 2 , Rongsheng Su 1
Affiliation
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Micro/nanoplastics (M/NPs) are the novel contaminants ubiquitous in the environment. Cadmium (Cd), a kind of heavy metal pollutant widely distributed, could potentially co-exist with PS-NPs in the environment. However, their combined effects on cardiomyocyte and its molecular mechanism in mammals remained ambiguous. Here, we examined whether PANoptosis, an emerging and complicated kind of programmed cell death, was involved in PS-NPs and Cd co-exposure-elicited cardiac injury. In this study, 60 male mice were orally subjected to environmentally relevant concentrations of PS-NPs (1 mg/kg) and/or CdCl (1.5 mg/kg) for 35 days. As we speculated, PS-NPs and Cd co-exposure affected the expression of pyroptosis(Caspase-1, Cleaved-Caspase-1, GSDMD, N-GSDMD, AIM2, Pyrin, NLRP3, IL-18, IL-1β)-, apoptosis(Caspase-3, Cleaved-Caspase-3, Caspase-8, Cleaved-Caspase-8, Caspase-7, BAX)- and necroptosis (t-RIPK3, p-RIPK3, t-RIPK1, p-RIPK1, t-MLKL, p-MLKL, ZBP1)-related genes and protein, resulting in growth restriction and damaged myocardial microstructure in mice. Notably, the combined effects on Cd and PS-NPs even predominantly aggravated the toxic damage. Intriguingly, we fortuitously discovered PS-NPs and/or Cd exposure facilitated linear ubiquitination of certain proteins in mice myocardium. In summation, this study shed light toward the effects of Cd and PS-NPs on cardiotoxicity, advanced the understanding of myocardial PANoptosis and provided a scientific foundation for further exploration of the combined toxicological effects of PS-NPs and heavy metals.
中文翻译:
聚苯乙烯纳米塑料与镉共暴露通过调节 PANoptosis 通路加重小鼠心肌细胞损伤
微/纳米塑料(M/NP)是环境中普遍存在的新型污染物。镉(Cd)是一种广泛分布的重金属污染物,有可能与环境中的PS-NP共存。然而,它们对哺乳动物心肌细胞的综合作用及其分子机制仍然不明确。在这里,我们检查了 PANoptosis(一种新兴且复杂的程序性细胞死亡)是否与 PS-NP 和 Cd 共同暴露引起的心脏损伤有关。在这项研究中,60 只雄性小鼠口服环境相关浓度的 PS-NP(1 毫克/千克)和/或 CdCl(1.5 毫克/千克)35 天。正如我们推测的,PS-NPs 和 Cd 共同暴露影响焦亡的表达(Caspase-1、Cleaved-Caspase-1、GSDMD、N-GSDMD、AIM2、Pyrin、NLRP3、IL-18、IL-1β)-、细胞凋亡(Caspase-3、Cleaved-Caspase-3、Caspase-8、Cleaved-Caspase-8、Caspase-7、BAX)- 和坏死性凋亡(t-RIPK3、p-RIPK3、t-RIPK1、p-RIPK1、t- MLKL、p-MLKL、ZBP1)相关基因和蛋白,导致小鼠生长受限和心肌微结构受损。值得注意的是,Cd 和 PS-NP 的综合作用甚至主要加剧了毒性损害。有趣的是,我们偶然发现 PS-NP 和/或 Cd 暴露促进了小鼠心肌中某些蛋白质的线性泛素化。总之,本研究揭示了Cd和PS-NPs对心脏毒性的影响,增进了对心肌全凋亡的认识,并为进一步探索PS-NPs和重金属的联合毒理学作用提供了科学基础。
更新日期:2024-03-08
中文翻译:
![](https://scdn.x-mol.com/jcss/images/paperTranslation.png)
聚苯乙烯纳米塑料与镉共暴露通过调节 PANoptosis 通路加重小鼠心肌细胞损伤
微/纳米塑料(M/NP)是环境中普遍存在的新型污染物。镉(Cd)是一种广泛分布的重金属污染物,有可能与环境中的PS-NP共存。然而,它们对哺乳动物心肌细胞的综合作用及其分子机制仍然不明确。在这里,我们检查了 PANoptosis(一种新兴且复杂的程序性细胞死亡)是否与 PS-NP 和 Cd 共同暴露引起的心脏损伤有关。在这项研究中,60 只雄性小鼠口服环境相关浓度的 PS-NP(1 毫克/千克)和/或 CdCl(1.5 毫克/千克)35 天。正如我们推测的,PS-NPs 和 Cd 共同暴露影响焦亡的表达(Caspase-1、Cleaved-Caspase-1、GSDMD、N-GSDMD、AIM2、Pyrin、NLRP3、IL-18、IL-1β)-、细胞凋亡(Caspase-3、Cleaved-Caspase-3、Caspase-8、Cleaved-Caspase-8、Caspase-7、BAX)- 和坏死性凋亡(t-RIPK3、p-RIPK3、t-RIPK1、p-RIPK1、t- MLKL、p-MLKL、ZBP1)相关基因和蛋白,导致小鼠生长受限和心肌微结构受损。值得注意的是,Cd 和 PS-NP 的综合作用甚至主要加剧了毒性损害。有趣的是,我们偶然发现 PS-NP 和/或 Cd 暴露促进了小鼠心肌中某些蛋白质的线性泛素化。总之,本研究揭示了Cd和PS-NPs对心脏毒性的影响,增进了对心肌全凋亡的认识,并为进一步探索PS-NPs和重金属的联合毒理学作用提供了科学基础。