Considering the unfavorable impacts of methyl viologen-induced oxidative stress (MV1-2, 50 and 500 µM) on growth, gas exchange (intercellular CO2 concentration, carbon assimilation rate, stomatal conductance, transpiration rate), the efficiency of PSII photochemistry and gene expressions of proteins related to photosystems, antioxidant capacity, and the content/histochemical staining of reactive oxygen species (ROS) markers, the experiment was conducted to evaluate the possible mechanisms of sodium hydrosulfide hydrate (a hydrogen sulfide donor, 500 µM NaHS) and its scavenger/inhibitor (hypotaurine, 50 µM and hydroxylamine, 100 µM) in Arabidopsis thaliana for 24 h. NaHS alleviated stress-reduced growth (4.2-fold increase for MV2 + NaHS) and improved the gas exchange parameters. NaHS was capable of improving the photosynthetic ability under 50 µM MV through sustaining photochemical activity in PSII and photochemical conversion efficiency as evident by transcript levels of psbA, psbD, psaA, and psaB. Stress-caused oxidative damage was scavenged by POX (a 90% increase). However, this action was not enough, suggested by increased ROS accumulation, lipid peroxidation (a 165% induction) and lipoxygenase activity (2.4-fold increase), and loss of membrane integrity. Meanwhile, NaHS successfully eliminated these responses against MV, evidenced by weak histochemical staining of ROS and lesser lipid peroxidation and membrane damage. The synchronized activities of both SOD and CAT triggered by NaHS were responsible for decreasing H2O2 content (by 57.4% decrease for MV2 + NaHS) in response to MV stress. After stress exposure, NaHS utilized the ascorbate–glutathione (AsA-GSH) cycle for removing H2O2. Arabidopsis subjected to MV1 plus NaHS exhibited the advanced levels of AsA regeneration (by 15.3% increase) and the redox state of GSH. Interestingly, NaHS under the high MV concentration did not maintain the re-establishment of GSH homeostasis and redox state of GSH in spite of the induced AsA/DHA (dehydroascorbate). NaHS could protect Arabidopsis from oxidative stress, likely by regulating growth, gas exchange, and photosynthetic performance, inducing expression levels of genes associated with photosystems and regulating antioxidant capacity, and redox balance for AsA and GSH.