Ozone is a secondary air pollutant, which causes oxidative stress in plants by producing reactive oxygen species (ROS) starting by an external attack of leaf apoplast. ROS have a dual role, acting as signaling molecules, regulating different physiological processes and response to stress, but also inducing oxidative damage. The production of ROS in plant cells is compartmented and regulated by scavengers and specific enzyme pathways. Chronic doses of ozone are known to trigger an important increase of the respiratory process while decreasing photosynthesis. Mitochondria, which normally operate with usual levels of intracellular ROS, would have to play a prominent role to cope with an enhanced ozone-derived ROS production. It is thus needed to compile the available literature on the effects of ozone on mitochondria to precise their strategy facing oxidative stress. An overview of the mitochondrial fate in three steps is proposed, i) starting with the initial responses of the mitochondria for alleviating the overproduction of ROS by the enhancement of existing antioxidant metabolism and adjustments of the electron transport chain, ii) followed by the setting up of detoxifying processes through exchanges between mitochondria and the cell, and iii) ending by an accelerated senescence initiated by mitochondrial membrane permeability and leading to programmed cell death.

臭氧是次要的空气污染物，会通过叶片质外体的外部攻击而产生活性氧（ROS），从而在植物中引起氧化应激。ROS具有双重作用，充当信号分子，调节不同的生理过程和对压力的反应，还诱导氧化损伤。植物细胞中活性氧的产生是通过清除剂和特定的酶途径来分隔和调节的。已知臭氧的长期剂量会触发呼吸过程的重要增加，同时降低光合作用。线粒体通常以通常水平的细胞内ROS运作，因此在应对臭氧衍生的ROS产生增加的过程中必须扮演重要角色。因此，需要汇编有关臭氧对线粒体影响的现有文献，以精确确定其面对氧化应激的策略。提出了对线粒体命运的三个步骤的概述，i）从线粒体的初始反应开始，以通过增强现有的抗氧化剂代谢和调节电子传输链来缓解ROS的过量产生； ii）随后进行设置通过线粒体与细胞之间的交换进行解毒过程，以及iii）以线粒体膜通透性引发的加速衰老结束并导致程序性细胞死亡。