Hydrogen sulfide-induced chilling resistance in peach fruit is performed via sustaining the homeostasis of ROS and RNS.

Hydrogen sulfide (H2S) application impacts on endogenous H2S, reactive oxygen species (ROS), and reactive nitrogen species (RNS) in cold-stored peach fruit were investigated. 20 μL L-1 H2S (NaHS as the donor) efficiently retarded the quality deterioration arising from chilling injury (CI), triggering endogenous H2S production, while enhancing antioxidant systems and ROS generation (NADPH oxidative enzyme). H2S promoted nitric oxide (NO) correlated with the S-nitrosoglutathione reductase (GSNOR)-mediated GSNO reduction, while suppressing the peroxynitrite anion content. As the pivotal coenzyme of ROS and RNS, nicotinamide adenine dinucleotide phosphate (NADPH) levels were elevated by H2S during late-stage storage via the tricarboxylic acid cycle, where reduced NADP-isocitrate dehydrogenase (NADP-ICDH) activity and gene expression. Structural analysis of peach NADP-ICDH (UniProtKB M5WXP5) deduced that Cys79 and Tyr396 are the likeliest targets for S-nitrosylation and nitration, respectively. These results indicate that H2S counteracts the disorders of ROS and RNS to ameliorate CI of peach fruit.