Journal
PLANT PHYSIOLOGY AND BIOCHEMISTRY
Volume 159, Issue -, Pages 202-210Publisher
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.plaphy.2020.12.019
Keywords
Ozone; Respiration; Mitochondria; Oxidative stress; ROS; Time-course response steps
Categories
Funding
- French National Research Agency through the Laboratory of Excellence ARBRE [ANR-12-LABXARBRE-01]
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Ozone as a secondary air pollutant can cause oxidative stress in plants by producing ROS, which have dual roles as signaling molecules and inducers of oxidative damage. Mitochondria play a crucial role in coping with ozone-induced ROS production and the mitochondrial fate involves three steps including initial responses, detoxifying processes, and accelerated senescence leading to programmed cell death.
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.
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