Key Laboratory of Cardiovascular Epidemiology & Department of Epidemiology, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Department of Critical Care Medicine, Yuhuangding Hospital, Qingdao University, Yantai, China.
Environ Toxicol. 2021 May;36(5):935-944. doi: 10.1002/tox.23095. Epub 2021 Jan 6.
The extensive existing of microplastics (MPs) in the ecosystem have increased considerable attention concerning their potential adverse effects, the toxicities and the underlying mechanism of MPs are still scarce. To explore the effect of MPs on cardiac tissue in Wistar rats and unravel the mechanism of pyroptosis and oxidative stress in the process of cardiomyocytes injury, 32 male Wister rats were divided into control group and three model groups, which were exposed to 0.5 mm PS MPs at 0.5, 5 and 50 mg/L for 90 days. Results revealed that MPs could damage cardiac structure and function with impaired mitochondria integrity, as well as increased levels of creatine kinase-MB and cardiac troponinI (cTnI). Moreover, MPs administration triggered oxidative stress as indicated by increased levels of malondialdehyde and decreased activity of superoxide dismutase, glutathione peroxidase and catalase. Treatment with MPs resulted in apoptosis and pyroptosis as evidenced by increasing expressions of interleukin (IL)-1β, IL-18. Additionally, MPs were shown to induce the NOD-like receptor protein 3 inflammasomes activation in cardiac tissue, enabling activation of Caspase-1-dependent signaling pathway induced by inflammatory stimuli resulting from oxidative stress. In summary, these results illustrated that pyroptosis played a vital role in polystyrene MPs-induced cardiotoxicity, which might be helpful to understand the mechanism of cardiac dysfunction and induced by MPs.
微塑料（MPs）在生态系统中的广泛存在引起了人们对其潜在不良影响的极大关注，但其毒性及其潜在机制仍知之甚少。为了探讨 MPs 对 Wistar 大鼠心脏组织的影响，揭示细胞焦亡和氧化应激在心肌损伤过程中的机制，将 32 只雄性 Wistar 大鼠分为对照组和 3 个模型组，分别暴露于 0.5mm PS MPs 浓度为 0.5、5 和 50mg/L 下 90 天。结果表明， MPs 可破坏心脏结构和功能，导致线粒体完整性受损，肌酸激酶同工酶-MB 和心肌肌钙蛋白 I（cTnI）水平升高。此外，MPs 给药会引发氧化应激，表现为丙二醛水平升高和超氧化物歧化酶、谷胱甘肽过氧化物酶和过氧化氢酶活性降低。MPs 处理会导致细胞凋亡和细胞焦亡，表现为白细胞介素（IL）-1β和 IL-18 表达增加。此外，研究表明 MPs 可在心脏组织中诱导 NOD 样受体蛋白 3 炎性小体的激活，从而激活由氧化应激引起的炎性刺激诱导的 Caspase-1 依赖性信号通路。总之，这些结果表明，细胞焦亡在聚苯乙烯 MPs 诱导的心脏毒性中起关键作用，这可能有助于理解 MPs 诱导的心脏功能障碍的机制。
