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      The Roles of Environmental Factors in Regulation of Oxidative Stress in Plant

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          Abstract

          Exposure to a variety of environmental factors such as salinity, drought, metal toxicity, extreme temperature, air pollutants, ultraviolet-B (UV-B) radiation, pesticides, and pathogen infection leads to subject oxidative stress in plants, which in turn affects multiple biological processes via reactive oxygen species (ROS) generation. ROS include hydroxyl radicals, singlet oxygen, and hydrogen peroxide in the plant cells and activates signaling pathways leading to some changes of physiological, biochemical, and molecular mechanisms in cellular metabolism. Excessive ROS, however, cause oxidative stress, a state of imbalance between the production of ROS and the neutralization of free radicals by antioxidants, resulting in damage of cellular components including lipids, nucleic acids, metabolites, and proteins, which finally leads to the death of cells in plants. Thus, maintaining a physiological level of ROS is crucial for aerobic organisms, which relies on the combined operation of enzymatic and nonenzymatic antioxidants. In order to improve plants' tolerance towards the harsh environment, it is vital to reinforce the comprehension of oxidative stress and antioxidant systems. In this review, recent findings on the metabolism of ROS as well as the antioxidative defense machinery are briefly updated. The latest findings on differential regulation of antioxidants at multiple levels under adverse environment are also discussed here.

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          The role of antioxidants in the chemistry of oxidative stress: A review.

          This Review Article is focused on the action of the reactive oxygenated species in inducing oxidative injury of the lipid membrane components, as well as on the ability of antioxidants (of different structures and sources, and following different mechanisms of action) in fighting against oxidative stress. Oxidative stress is defined as an excessive production of reactive oxygenated species that cannot be counteracted by the action of antioxidants, but also as a perturbation of cell redox balance. Reactive oxygenated/nitrogenated species are represented by superoxide anion radical, hydroxyl, alkoxyl and lipid peroxyl radicals, nitric oxide and peroxynitrite. Oxidative stress determines structure modifications and function modulation in nucleic acids, lipids and proteins. Oxidative degradation of lipids yields malondialdehyde and 4-hydroxynonenal, but also isoprostanes, from unsaturated fatty acids. Protein damage may occur with thiol oxidation, carbonylation, side-chain oxidation, fragmentation, unfolding and misfolding, resulting activity loss. 8-hydroxydeoxyguanosine is an index of DNA damage. The involvement of the reactive oxygenated/nitrogenated species in disease occurrence is described. The unbalance between the oxidant species and the antioxidant defense system may trigger specific factors responsible for oxidative damage in the cell: over-expression of oncogene genes, generation of mutagen compounds, promotion of atherogenic activity, senile plaque occurrence or inflammation. This leads to cancer, neurodegeneration, cardiovascular diseases, diabetes, kidney diseases. The concept of antioxidant is defined, along with a discussion of the existent classification criteria: enzymatic and non-enzymatic, preventative or repair-systems, endogenous and exogenous, primary and secondary, hydrosoluble and liposoluble, natural or synthetic. Primary antioxidants are mainly chain breakers, able to scavenge radical species by hydrogen donation. Secondary antioxidants are singlet oxygen quenchers, peroxide decomposers, metal chelators, oxidative enzyme inhibitors or UV radiation absorbers. The specific mechanism of action of the most important representatives of each antioxidant class (endogenous and exogenous) in preventing or inhibiting particular factors leading to oxidative injury in the cell, is then reviewed. Mutual influences, including synergistic effects are presented and discussed. Prooxidative influences likely to occur, as for instance in the presence of transition metal ions, are also reminded.
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            Lipid peroxidation in cell death.

            Disruption of redox homeostasis is a key phenotype of many pathological conditions. Though multiple oxidizing compounds such as hydrogen peroxide are widely recognized as mediators and inducers of oxidative stress, increasingly, attention is focused on the role of lipid hydroperoxides as critical mediators of death and disease. As the main component of cellular membranes, lipids have an indispensible role in maintaining the structural integrity of cells. Excessive oxidation of lipids alters the physical properties of cellular membranes and can cause covalent modification of proteins and nucleic acids. This review discusses the synthesis, toxicity, degradation, and detection of lipid peroxides in biological systems. Additionally, the role of lipid peroxidation is highlighted in cell death and disease, and strategies to control the accumulation of lipid peroxides are discussed.
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              Regulation of pattern recognition receptor signalling in plants.

              Recognition of pathogen-derived molecules by pattern recognition receptors (PRRs) is a common feature of both animal and plant innate immune systems. In plants, PRR signalling is initiated at the cell surface by kinase complexes, resulting in the activation of immune responses that ward off microorganisms. However, the activation and amplitude of innate immune responses must be tightly controlled. In this Review, we summarize our knowledge of the early signalling events that follow PRR activation and describe the mechanisms that fine-tune immune signalling to maintain immune homeostasis. We also illustrate the mechanisms used by pathogens to inhibit innate immune signalling and discuss how the innate ability of plant cells to monitor the integrity of key immune components can lead to autoimmune phenotypes following genetic or pathogen-induced perturbations of these components.
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                Author and article information

                Contributors
                Journal
                Biomed Res Int
                Biomed Res Int
                BMRI
                BioMed Research International
                Hindawi
                2314-6133
                2314-6141
                2019
                8 May 2019
                : 2019
                : 9732325
                Affiliations
                1School of Life Sciences, Sichuan Agricultural University, Ya'an 625014, China
                2Institute of Ecological Agriculture, Sichuan Agricultural University, Chengdu 611130, China
                Author notes

                Guest Editor: Hengjia Ni

                Author information
                http://orcid.org/0000-0002-9152-9211
                Article
                10.1155/2019/9732325
                6530150
                31205950
                b879d37a-9d4f-47a0-839d-fcc67ae08418
                Copyright © 2019 Xiulan Xie et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 26 February 2019
                : 16 April 2019
                Funding
                Funded by: National Natural Science Foundation of China
                Award ID: 31801839
                Funded by: Henry Fok Foundation
                Award ID: 151104
                Funded by: Ministry of Human Resources and Social Security, China
                Funded by: Sichuan Provincial Department of Science and Technology, China
                Award ID: 2018HH0042
                Award ID: 2016JQ0009
                Funded by: Sichuan Provincial Department of Education, China
                Award ID: 16TD0005
                Award ID: 15ZA0001
                Categories
                Review Article

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