Institutes of Agricultural Science and Technology Development (Joint International Research laboratory of Agriculture and Agri-Product Safety of the Ministry of Education of China)/College of Veterinary Medicine, Yangzhou University, Yangzhou, 225009, China.
Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou, 225009, China.
Environ Toxicol. 2023 Aug;38(8):1775-1785. doi: 10.1002/tox.23804. Epub 2023 Apr 6.
Cadmium (Cd) is an environmental heavy metal, and its accumulation is harmful to animal and human health. The cytotoxicity of Cd includes oxidative stress, apoptosis, and mitochondrial histopathological changes. Furthermore, polystyrene (PS) is a kind of microplastic piece derived from biotic and abiotic weathering courses, and has toxicity in various aspects. However, the potential mechanism of action of Cd co-treated with PS is still poorly unclear. The objective of this study was to investigate the effects of PS on Cd-induced histopathological injury of mitochondria in the lung of mice. In this study, the results have showed that Cd could induce the activity of oxidative enzymes of the lung cells in mice, increasing the content of partial microelement and the phosphorylation of inflammatory factor NF-κB p65. Cd further destroys the integrity of mitochondria by increasing the expression of apoptotic protein and blocking the autophagy. In addition, PS solely group aggravated the lung damage in mice, especially mitochondrial toxicity, and played a synergistic effect with Cd in lung injury. However, how PS can augment mitochondrial damage and synergism with Cd in lung of mice requiring further exploration. Therefore, PS was able to exacerbate Cd-induced mitochondrial damage to the lung in mice by blocking autophagy, and was associated with the apoptosis.
镉 (Cd) 是一种环境重金属，其积累对动物和人类健康有害。镉的细胞毒性包括氧化应激、细胞凋亡和线粒体组织病理学变化。此外，聚苯乙烯 (PS) 是一种源自生物和非生物风化过程的微塑料碎片，在各个方面都具有毒性。然而，Cd 与 PS 共同处理的潜在作用机制仍不清楚。本研究旨在探讨 PS 对 Cd 诱导的小鼠肺线粒体组织病理学损伤的影响。在这项研究中，结果表明 Cd 可诱导小鼠肺细胞的氧化酶活性，增加部分微量元素的含量和炎性因子 NF-κB p65 的磷酸化。Cd 进一步通过增加凋亡蛋白的表达和阻断自噬来破坏线粒体的完整性。此外，PS 单独组加重了小鼠的肺部损伤，特别是线粒体毒性，并与 Cd 在肺部损伤中表现出协同作用。然而，PS 如何在小鼠的肺部中增强与 Cd 协同作用的线粒体损伤，还需要进一步探索。因此，PS 通过阻断自噬来加剧 Cd 诱导的小鼠肺线粒体损伤，并与凋亡有关。
