3-氯-1,2-丙二醇酯通过 CTSB/TFAM/ROS 通路诱导 HepG2 细胞发生坏死性凋亡。
3-Monochloropropane-1,2-diol esters induce HepG2 cells necroptosis via CTSB/TFAM/ROS pathway.
机构信息
College of Food Science and Engineering, Jilin University, Changchun, Jilin, 130062, People's Republic of China; Key Laboratory of Zoonosis, Ministry of Education College of Veterinary Medicine, Jilin University, Changchun, Jilin, 130062, People's Republic of China.
College of Food Science and Engineering, Jilin University, Changchun, Jilin, 130062, People's Republic of China.
出版信息
Food Chem Toxicol. 2024 Apr;186:114525. doi: 10.1016/j.fct.2024.114525. Epub 2024 Feb 24.
3-monochloropropane-1,2-diol esters (3-MCPDE) are toxic substances that form in food thermal processing and have a diverse range of toxicities. In this study, we found that 3-MCPDE triggered necroptosis by RIPK1/RIPK3/MLKL pathway in HepG2 cells. Previous studies have shown that ROS is an important activator of RIPK1 and RIPK3. The data showed that 3-MCPDE induced excessive ROS production through mitochondrial damage. After treatment with ROS inhibitor N-acetylcysteine (NAC), 3-MCPDE-induced necroptosis was relieved. Further, we explored how 3-MCPDE destroys mitochondria. The data suggested that 3-MCPDE induced mitochondrial dysfunction through the CTSB/TFAM pathway. Overall, the results indicated that 3-MCPDE induced necroptosis through CTSB/TFAM/ROS pathway in HepG2 cells. Our study provided a new mechanism for 3-MCPDE hepatotoxicity.
3-单氯丙二醇酯（3-MCPDE）是在食品热加工过程中形成的有毒物质，具有多种毒性。在本研究中，我们发现 3-MCPDE 通过 RIPK1/RIPK3/MLKL 途径在 HepG2 细胞中引发坏死性凋亡。先前的研究表明，ROS 是 RIPK1 和 RIPK3 的重要激活剂。数据显示，3-MCPDE 通过线粒体损伤诱导过量 ROS 的产生。用 ROS 抑制剂 N-乙酰半胱氨酸（NAC）处理后，缓解了 3-MCPDE 诱导的坏死性凋亡。此外，我们探讨了 3-MCPDE 如何破坏线粒体。数据表明，3-MCPDE 通过 CTSB/TFAM 途径诱导线粒体功能障碍。总体而言，结果表明 3-MCPDE 通过 CTSB/TFAM/ROS 途径在 HepG2 细胞中诱导坏死性凋亡。我们的研究为 3-MCPDE 的肝毒性提供了新的机制。
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