Reactive oxygen species (ROS, partial reduction or derivatives of free radicals) are highly reactive, dangerous and can cause oxidative cell death. In addition to their role as toxic by-products of aerobic metabolism, ROS play a role in the control and regulation of biological processes such as growth, the cell cycle, programmed cell death, hormone signaling, biotic and abiotic stress reactions and development. ROS always arise in plants as a by-product of several metabolic processes that are located in different cell compartments, or as a result of the inevitable escape of electrons to oxygen from the electron transport activities of chloroplasts, mitochondria and plasma membranes. These reactive species are formed in chloroplasts, mitochondria, plasma membranes, peroxisomes, apoplasts, the endoplasmic reticulum and cell walls. The action of many non-enzymatic and enzymatic antioxidants present in tissues is required for efficient scavenging of ROS generated during various environmental stressors. The current review provides an in-depth look at the fate of ROS in plants, a beneficial role in managing stress and other irregularities. The production sites are also explained with their negative effects. In addition, the biochemical properties and sources of ROS generation, capture systems, the influence of ROS on cell biochemistry and the crosstalk of ROS with other signaling molecules/pathways are discussed.

This work was designed to evaluate whether external application of nitric oxide (NO) in the form of its donor S-nitroso-N-acetylpenicillamine (SNAP) could mitigate the deleterious effects of NaCl stress on chickpea (Cicer arietinum L.) plants. SNAP (50 μM) was applied to chickpea plants grown under non-saline and saline conditions (50 and 100 mM NaCl). Salt stress inhibited growth and biomass yield, leaf relative water content (LRWC) and chlorophyll content of chickpea plants. High salinity increased electrolyte leakage, carotenoid content and the levels of osmolytes (proline, glycine betaine, soluble proteins and soluble sugars), hydrogen peroxide (H₂O₂) and malondialdehyde (MDA), as well as the activities of antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), and glutathione reductase in chickpea plants. Expression of the representative SOD, CAT and APX genes examined was also up-regulated in chickpea plants by salt stress. On the other hand, exogenous application of NO to salinized plants enhanced the growth parameters, LRWC, photosynthetic pigment production and levels of osmolytes, as well as the activities of examined antioxidant enzymes which is correlated with up-regulation of the examined SOD, CAT and APX genes, in comparison with plants treated with NaCl only. Furthermore, electrolyte leakage, H₂O₂ and MDA contents showed decline in salt-stressed plants supplemented with NO as compared with those in NaCl-treated plants alone. Thus, the exogenous application of NO protected chickpea plants against salt stress-induced oxidative damage by enhancing the biosyntheses of antioxidant enzymes, thereby improving plant growth under saline stress. Taken together, our results demonstrate that NO has capability to mitigate the adverse effects of high salinity on chickpea plants by improving LRWC, photosynthetic pigment biosyntheses, osmolyte accumulation and antioxidative defense system.

Although trace elements are essential for life, environmental contamination due to metal accumulation and overuse in various sectors, such as healthcare, agriculture, industry, and cosmetics, poses significant health concerns. Exposure of plants to heavy metals leads to the overproduction of reactive oxygen species (ROS) due to their ability to change mitochondrial membrane permeability and restrict the action of ROS clearance enzymes in the cellular antioxidant system. The interaction of ROS with cellular membranes, heavy-metal-induced interactions directly or indirectly with different macromolecules, and signaling pathways leads to the accumulation of environmental pollutants and oxidative stress in exposed organisms. The heavy metal–ROS–cell signaling axis affects various pathological processes such as ATP depletion, excess ROS production, mitochondrial respiratory chain damage, decoupling of oxidative phosphorylation, and mitochondrial death. This review focuses on discussing the toxic effects of different heavy metals on plants, with particular emphasis on oxidative stress, its consequences, and mitigation strategies.