Abstract
Sulfur dioxide (SO2) is a major air pollutant and has significant impacts on plant physiology. Plant can adapt to SO2 stress by controlling stomatal movement, gene expression, and metabolic changes. Here we show clear evidences that SO2-triggered hydrogen peroxide (H2O2) production mediated stomatal closure and cell death in Arabidopsis leaves. High levels of SO2 caused irreversible stomatal closure and decline in guard cell viability, but low levels of SO2 caused reversible stomatal closure. Exogenous antioxidants ascorbic acid (AsA) and catalase (CAT) or Ca2+ antagonists EGTA and LaCl3 blocked SO2-induced stomatal closure and decline in viability. AsA and CAT also blocked SO2-induced H2O2 and [Ca2+]cyt elevation. However, EGTA and LaCl3 inhibited SO2-induced [Ca2+]cyt increase but did not suppress SO2-induced H2O2 elevation. These results indicate that H2O2 elevation triggered stomatal closure and cell death via [Ca2+]cyt signaling in SO2-stimulated Arabidopsis guard cells. NADPH oxidase inhibitor DPI blocked SO2-induced cell death but not the stomatal closure triggered by low levels of SO2, indicating that NADPH oxidase-dependent H2O2 production plays critical role in SO2 toxicity but is not necessary for SO2-induced stomatal closure. Our results suggest that H2O2 production and accumulation in SO2-stimulated plants trigger plant adaptation and toxicity via reactive oxygen species mediating Ca2+ signaling.
Highlights
Sulfur dioxide (SO2) is a harmful gas that is emitted largely from burning coal, high-sulfur oil, and fuels
Application of DPI, which is widely accepted as a relatively specific direct inhibitor of NADPH oxidase, markedly blocked SO2-induced cell death but cannot suppress stomatal closure evoked by low concentrations of SO2. These findings indicate that H2O2mediated stomatal closure in Arabidopsis leaves exposed to low concentrations of SO2 is not dependent on the activity of plasma membrane NADPH oxidase, but cell death evoked by high concentrations of SO2 is NADPH oxidase-dependent
H2O2 elevation triggered by SO2 mediated both stomatal closure and cell death via Ca2+ signaling
Summary
Sulfur dioxide (SO2) is a harmful gas that is emitted largely from burning coal, high-sulfur oil, and fuels. High levels of SO2 can injure many plant species and varieties, resulting in photosynthesis decline, growth inhibition, and even death [1,2,3,4]. Sulfur dioxide enters plants mainly through the open stomata [5]. Once it enters the leaf, SO2 is hydrated to form HSO3− and SO32−. The toxicity of SO2 is derived from molecular species sulfite (SO32−) and bisulfite (HSO3−) generated after SO2 is dissolved in cellular fluid [6]. Sulfite oxidation, which is the detoxification reaction of sulfite to sulfate (SO42−), leads to the formation of reactive oxygen species (ROS) in plant cells [7, 8]. The production and accumulation of ROS are one of the key events in plant response to SO2 [9,10,11,12]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
