Up-regulation of nitrogen metabolism and chlorophyll biosynthesis by hydrogen sulfide improved photosystem photochemistry and gas exchange in chromium-contaminated bean (Phaseolus vulgaris L.) plants.

Hydrogen sulfide (H₂S) is considered as plant growth promoter under heavy metal stress, though its specific effects on photosynthesis are rarely explored. This study investigates the protective effects of exogenous H2S donor sodium hydrosulfide (NaHS) on chlorophyll metabolism and photosystem II (PSII) function in 24-day-old bean plants exposed to 10 μM chromium (Cr) stress. Sodium hydrosulfide (100 μM) reduced Cr accumulation in both roots and leaves, leading to restored plant growth. Concomitantly, H₂S mitigated Cr-induced oxidative damages by decreasing reactive oxygen species levels and further enhancing antioxidant scavenging activities. This resulted in significant reductions in Cr-elevated leaf pheophytin and chlorophyllide levels by 59% and 67%, respectively. Furthermore, NaHS application increased levels of porphyrin and its precursor, 5-aminolevulinic acid (5-ALA), in Cr-stressed bean. The up-regulation in chlorophyll biosynthesis was associated with enhanced activities of glutamine synthetase and glutamate synthase, essential for glutamate (precursor of 5-ALA) production, as well as nitrate and nitrite reductase, leading to increased nitric oxide generation. Under Cr stress, H₂S significantly improved the electron transport rate, effective quantum yield of PSII, and photochemical quenching by 112%, 53%, and 38%, respectively, while reducing non-photochemical quenching by 50%. Furthermore, H₂S promoted net CO₂ assimilation and photosynthesis at saturating light, respectively, while reducing stomatal conductance and transpiration to maintain water balance. Exogenous H₂S restored respiration, as indicated by increased light saturation and compensation points in Cr-treated plants. Overall, these findings indicate that H₂S regulates photosynthesis in Cr-stressed bean by modulating nitrogen and chlorophyll metabolism, thereby optimizing PSII efficiency and gas exchange.