Ma Long, Dong Jia-Xin, Wu Can, Li Xue-Yi, Chen Jing, Zhang Hong, Liu Yi
StateKey Laboratory for the Chemistry and Molecular Engineering of Medicinal Resources, School of Chemistry and Pharmaceutical Sciences, Guangxi Normal University, Guilin, 541004, People's Republic of China.
State Key Laboratory of Virology & Key Laboratory of Analytical Chemistry for Biology and Medicine (MOE), College of Chemistry and Molecular Sciences, Wuhan University, Wuhan, 430072, People's Republic of China.
J Membr Biol. 2017 Apr;250(2):195-204. doi: 10.1007/s00232-017-9947-0. Epub 2017 Feb 21.
Liver mitochondria are involved in several important life processes; mitochondrial dysfunction and disorders are implicated in several human diseases. Alcohol permeates all tissues of the body and exerts some intrinsic hepatotoxicity. In this work, our results demonstrated that ethanol caused a series of mitochondria permeability transition pore (MPTP) opening factors such as mitochondrial swelling, increased permeability of H and K, collapsed membrane potential, and increased membrane fluidity. Furthermore, mitochondrial ultrastructure alternation observed clearly by transmission electron microscopy and the release of Cytochrome c could explain the MPTP opening from another aspect. Moreover, ethanol damaged the mitochondrial respiration system and induced disturbance of mitochondrial energy metabolism which was monitored by polarographic and microcalorimetric methods, respectively. Considered together, these damages may promote both apoptotic and necrotic cell death and contribute to the onset or progression alcohol-induced liver diseases.
肝脏线粒体参与多个重要生命过程；线粒体功能障碍与多种人类疾病有关。酒精可渗透至身体所有组织，并具有一定的内在肝毒性。在本研究中，我们的结果表明，乙醇会引发一系列线粒体通透性转换孔（MPTP）开放因素，如线粒体肿胀、H⁺和K⁺通透性增加、膜电位崩溃以及膜流动性增加。此外，通过透射电子显微镜清晰观察到的线粒体超微结构改变以及细胞色素c的释放，可从另一个角度解释MPTP的开放。此外，乙醇破坏了线粒体呼吸体系，并分别通过极谱法和微量量热法监测到其诱导线粒体能量代谢紊乱。综合来看，这些损伤可能会促进细胞凋亡和坏死性死亡，并导致酒精性肝病的发生或进展。
