线粒体
细胞生物学
氧化应激
线粒体ROS
粒体自噬
活性氧
氧化磷酸化
上睑下垂
自噬
化学
生物
程序性细胞死亡
细胞凋亡
生物化学
作者
Tingting Wu,Zhigang Li,Yongjie Wei
标识
DOI:10.1016/j.scitotenv.2022.160589
摘要
Mitochondria are double-membraned organelles found in eukaryotic cells. The integrity of mitochondrial structure and function determines cell destiny. Mitochondria are also the "energy factories of cells." The production of energy is accompanied by reactive oxygen species (ROS) generation. Generally, the production and consumption of ROS maintains a balance in cells. Ozone is a highly oxidizing, harmful substance in ground-level atmosphere. Ozone inhalation causes oxidative injury owing to the generation of ROS, resulting in mitochondrial oxidative stress overload. Oxidative damage to the mitochondria induces a vicious cycle of ROS production which might destroy mitochondrial DNA and mitochondrial structure and function in cells. ROS can alter the phosphorylation of various signaling molecules, triggering a series of downstream signaling pathway reactions. These include inflammatory responses, pyroptosis, autophagy, and apoptosis. Changes involving these molecular mechanisms may be related to the occurrence of disease. According to numerous epidemiological investigations, ozone exposure induces respiratory, cardiovascular, and nervous system diseases in humans. In addition, these systems require large quantities of energy. Hence, the mitochondrial damage caused by ozone may act as a bridge between human diseases. However, the specific molecular mechanisms involved require further investigation. This review discusses our understanding of the structure and function of mitochondria the mechanisms underlying ozone-induced mitochondrial damage.
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