Modification of Chloroplast Antioxidant Capacity by Plastid Transformation.

As immobile organisms, green plants must be frequently challenged by a broad range of environmental stresses. During these constantly adverse conditions, reactive oxygen species (ROS) levels can rise extremely in plants, leading to cellular dysfunction and cell death presumably due to irreversible protein overoxidation. Once considered merely as deleterious molecules, cells seek to remove them as efficiently as possible. To enhance ROS scavenging capacity, genes encoding antioxidative enzymes can be directly expressed from the genome of plastid (chloroplast), a major compartment for ROS production in photosynthetic organisms. Thus, overexpression of antioxidant enzymes by plastid engineering may provide an alternative to enhance plant's tolerance to stressful conditions specifically related with chloroplast-derived ROS. Here, we describe basic procedures for expressing glutathione reductase, a vital component of ascorbate-glutathione pathway, in tobacco via plastid transformation technology.

Hydrogen sulfide attenuates intracellular oxidative stress via repressing glycolate oxidase activities in Arabidopsis thaliana.

BACKGROUND: Hydrogen sulfide (H2S) has been proposed to exert anti-oxidative effect under many environmental stresses; however, how it influences oxidative stress remains largely unclear. RESULTS: Here, we assessed the effects of H2S on oxidative stress responses such as salicylic acid (SA)-dependent cell death, which triggered by increased H2O2 availability in Arabidopsis thaliana catalase-deficient mutants cat2 displaying around 20% wild-type catalase activity. H2S generation and its producing enzyme L-cysteine desulfhydrase (LCD/DES) were found to transient increase in response to intracellular oxidative stress. Although introducing the mutation of des1, an important LCD, into the cat2 background produced little effect, H2S fumigation not only rescued the cell death phenotype of cat2 plant, but also attenuated SA accumulation and oxidation of the glutathione pool. Unexpectedly, the activities of major components of ascorbate-glutathione pathway were less affected by the presence of H2S treatment, but decreased glycolate oxidase (GOX) in combination with accumulation of glycolate implied H2S treatment impacts the cellular redox homeostasis by repressing the GOX-catalyzed reaction likely via altering the major GOX transcript levels. CONCLUSIONS: Our findings reveal a link between H2S and peroxisomal H2O2 production that has implications for the understanding of the multifaceted roles of H2S in the regulation of oxidative stress responses.

Abiotic stress-triggered oxidative challenges: Where does H2S act?

Hydrogen sulfide (H2S) was once principally considered the perpetrator of plant growth cessation and cell death. However, this has become an antiquated view, with cumulative evidence showing that the H2S serves as a biological signaling molecule notably involved in abiotic stress response and adaptation, such as defense by phytohormone activation, stomatal movement, gene reprogramming, and plant growth modulation. Reactive oxygen species (ROS)-dependent oxidative stress is involved in these responses. Remarkably, an ever-growing body of evidence indicates that H2S can directly interact with ROS processing systems in a redox-dependent manner, while it has been gradually recognized that H2S-based posttranslational modifications of key protein cysteine residues determine stress responses. Furthermore, the reciprocal interplay between H2S and nitric oxide (NO) in regulating oxidative stress has significant importance. The interaction of H2S with NO and ROS during acclimation to abiotic stress may vary from synergism to antagonism. However, the molecular pathways and factors involved remain to be identified. This review not only aims to provide updated information on H2S action in regulating ROS-dependent redox homeostasis and signaling, but also discusses the mechanisms of H2S-dependent regulation in the context of oxidative stress elicited by environmental cues.