Reactive Oxygen Species in Chloroplasts and Chloroplast Antioxidants Under Abiotic Stress

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Background

An unavoidable consequence of aerobic metabolism by living cells is the production of reactive oxygen species (ROS) as regular cellular metabolic by-products. Plant cellular metabolism is continuously producing ROS such as superoxide anion radical (O2•–), hydrogen peroxide (H2O2), and singlet oxygen (1O2) at basal levels that are incapable to cause damage, as they are being scavenged by different antioxidant mechanisms. Environmental stresses such as metal toxicity, salinity, drought, chilling, and UV-B radiation lead to an enhancement of ROS (1O2, O2•–, H2O2, OH•) generation in plants due to disturbance of cellular homeostasis that can lead to oxidative stress. Oxidative stress results from the imbalance between the production of ROS and the scavenging of their reactive intermediates by antioxidants (enzymatic and non-enzymatic), causing cellular damage that can lead to cell death. Thus, the response of plants to this imbalance before the damage of their cellular structures is critical for maintaining high rates of photosynthesis and also for their survival.

Chloroplasts are considered as one of the most important producers of ROS in plant cells and more specific the light reactions of photosynthesis. Under most abiotic stresses the absorbed light energy exceeds what can be used and thus it can damage the photosynthetic apparatus. If this excess excitation energy is not quenched by the photoprotective mechanism of non-photochemical quenching (NPQ), increased production of ROS occurs that can lead to oxidative stress. Abiotic stress-induced ROS accumulation is scavenged by enzymatic antioxidants, such as superoxide dismutase (SOD), ascorbate peroxidase (APX), monodehydroascorbate reductase, (MDHAR), dehydroascorbate reductase (DHAR), glutathione reductase (GR), glutathione peroxidase, (GPX), guaiacol peroxidase (GOPX), glutathione-S- transferase (GST), and catalase (CAT), and non-enzymatic metabolites, such as ascorbic acid, glutathione, a-tocopherol, carotenoids, phenolic compounds, flavonoids, and proline.

Despite their destructive activity, ROS are well-described as second messengers in a variety of developmental and cellular processes including resilience to abiotic stresses. The role of chloroplast antioxidants, which often have overlying or interrelating functions, is not to totally eliminate O2•–, H2O2 and 1O2, but rather to achieve an appropriate balance between production and elimination in order to match the operation of photosynthesis and permit an efficient spread of signals to the nucleus. Singlet oxygen and H2O2 give rise to independent footprints, which usually are not antagonistic. These chloroplast-derived oxidative signals could activate regulatory networks to facilitate plant sensing and response to biotic and abiotic stress conditions. ROS not only activate the plant’s defense mechanisms in order to cope with the oxidative stress but also are essential for redox sensing, signaling, and regulation of a plethora of physiological functions tightly accomplishing plant function and development.

In this research topic, we aim for an article collection that explores the mechanism through which plant and allied photosynthetic organisms produce, utilize and eliminates ROS in plastid under abiotic stress. All article types published by Frontiers in Plant Science are welcome.

Please note: Frontiers in Plant Science does not accept solely descriptive studies - studies which report responses to treatments and descriptive reports of ‘Omics studies will not be considered if they do not progress biological understanding of these responses.

Keywords: Oxidative Stress, Reactive Oxygen Species, Redox, Abiotic Stress, Chloroplast

Important note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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