Читать книгу Nitric Oxide in Plants - Группа авторов - Страница 30

Sunlight is the principal source of energy for plants, and a portion of this energy exists in the form of ultraviolet (UV) radiation. It is typically partitioned into three categories: (i) UV-A (315–400 nm), (ii) UV-B (280–315 nm), and (iii) UV-C (200–280 nm). It is well known that the atmospheric gases completely absorb UV-C radiation, while UV-B rays are moderately absorbed by tropospheric ozone, and only a trivial fraction is transferred to the surface, and UV-A is scarcely absorbed by the ozone. Since the destruction of the ozone layer, the levels of UV-B radiation rise on the Earth’s surface. UV-B has high energy and induces production of ROS that employ harmful morphological and molecular changes in plants (Simontacchi et al. 2015). Chloroplasts are highly affected by UV-B radiation and the light-induced impairment is directed primarily to photosystem II (PSII), with the inhibition of the respiratory chain and oxidative damage to the D1 protein. UV-B treatment increased leakage of ions, hydrogen peroxide levels, and oxidation of thylakoid membrane protein in bean (Phaseolus vulgaris) leaves. It was also observed that the proficiency of PSII photochemistry (F _v/F _m) and the considerable production of PSII was decreased under UV radiation. But after exposure to NO, carbonyl groups of thylakoid membrane and levels of H₂O₂ were decreased. Thus, NO could exert a protective role against protein oxidation under stress conditions as was previously reported regarding lipid oxidation (Vanhaelewyn et al. 2016; Mannucci et al. 2020).

UV-B adversely affects the chloroplast and mesophyll cells of a plant. It has been reported that UV-B increases the level of plant hormone ABA, activates the NADPH oxidase, and generates H₂O₂. Pretreatment with apocynin (an inhibitor of NADPH oxidase), minimizes the UV-B-induced oxidative damage by reducing the breakdown of chlorophyll (Tewari et al. 2013; Bajguz 2014).

Ozone is formed by a photochemical reaction in NOx and volatile organic compounds (VOCs) and enters the plants through stomata where it accumulates in parenchyma tissues. As a pollutant, it affects the plant by generating oxidative stress via releasing ROS, e.g. superoxide O²⁻, singlet oxygen, hydroxyl radicals, and hydrogen peroxide in the plant cells. This oxidative stress can further damage the DNA, carbohydrate, lipids, and proteins (Vaultier and Jolivet 2015; Li et al. 2018). The contribution of NO in response to UV-B rays acts through ABA-mediated pathways (Xu et al. 2012). It has been proposed that in plant cells, UV-B radiation stress leads to an increase in ABA levels, which stimulates an increase in cytosolic Ca²⁺ concentration that ultimately starts NO production via NOS and/or NOS-like activities. This increase in NO production increase a plant’s tolerance for higher doses of UV-B indirectly by protecting cell redox homeostasis from uncontrolled generation of ROS and associated deleterious effects provoked by UV-B radiation.