Plants are constantly challenged by various abiotic stresses that negatively affect growth and productivity worldwide. During the course of their evolution, plants have developed sophisticated mechanisms to recognize external signals allowing them to respond appropriately to environmental conditions, although the degree of adjustability or tolerance to specific stresses differs from species to species. Overproduction of reactive oxygen species (ROS; hydrogen peroxide, H₂O₂; superoxide, ${\mathrm{O}}_{\mathrm{2}}^{\mathrm{\cdot -}}$; hydroxyl radical, OH^⋅ and singlet oxygen, ¹O₂) is enhanced under abiotic and/or biotic stresses, which can cause oxidative damage to plant macromolecules and cell structures, leading to inhibition of plant growth and development, or to death. Among the various ROS, freely diffusible and relatively long-lived H₂O₂ acts as a central player in stress signal transduction pathways. These pathways can then activate multiple acclamatory responses that reinforce resistance to various abiotic and biotic stressors. To utilize H₂O₂ as a signaling molecule, non-toxic levels must be maintained in a delicate balancing act between H₂O₂ production and scavenging. Several recent studies have demonstrated that the H₂O₂-priming can enhance abiotic stress tolerance by modulating ROS detoxification and by regulating multiple stress-responsive pathways and gene expression. Despite the importance of the H₂O₂-priming, little is known about how this process improves the tolerance of plants to stress. Understanding the mechanisms of H₂O₂-priming-induced abiotic stress tolerance will be valuable for identifying biotechnological strategies to improve abiotic stress tolerance in crop plants. This review is an overview of our current knowledge of the possible mechanisms associated with H₂O₂-induced abiotic oxidative stress tolerance in plants, with special reference to antioxidant metabolism.

Heavy metal (HM) toxicity is one of the major abiotic stresses leading to hazardous effects in plants. A common consequence of HM toxicity is the excessive accumulation of reactive oxygen species (ROS) and methylglyoxal (MG), both of which can cause peroxidation of lipids, oxidation of protein, inactivation of enzymes, DNA damage and/or interact with other vital constituents of plant cells. Higher plants have evolved a sophisticated antioxidant defense system and a glyoxalase system to scavenge ROS and MG. In addition, HMs that enter the cell may be sequestered by amino acids, organic acids, glutathione (GSH), or by specific metal-binding ligands. Being a central molecule of both the antioxidant defense system and the glyoxalase system, GSH is involved in both direct and indirect control of ROS and MG and their reaction products in plant cells, thus protecting the plant from HM-induced oxidative damage. Recent plant molecular studies have shown that GSH by itself and its metabolizing enzymes—notably glutathioneS-transferase, glutathione peroxidase, dehydroascorbate reductase, glutathione reductase, glyoxalase I and glyoxalase II—act additively and coordinately for efficient protection against ROS- and MG-induced damage in addition to detoxification, complexation, chelation and compartmentation of HMs. The aim of this review is to integrate a recent understanding of physiological and biochemical mechanisms of HM-induced plant stress response and tolerance based on the findings of current plant molecular biology research.