Interactive effects of H2O2 and NO on mitochondrial function and oxidative mtDNA damage in cold-stored peach fruit.

Hydrogen peroxide (H2O2) and nitric oxide (NO), as bioactive species, play critical regulatory roles in plants and correlate with each other under physiological and stressful conditions. The protective effect of NO has been demonstrated through the enhancement of the antioxidative system and the alleviation of oxidative mitochondrial DNA (mtDNA) damage in mitochondria under cold stress. To investigate the effect of H2O2 on mitochondrial function and mtDNA damage in cold-stored peaches and elucidate the interactive effects of H2O2 and NO, sodium nitroprusside (SNP, an NO donor) -pretreated peaches were further treated with H2O2 and the scavenger of reactive oxygen species (N-acetyl cysteine, NAC). Treatment with H2O2 significantly increased endogenous ROS content, raised levels of 8-hydroxyguanosine (8-OHdG) and apurinic/apyrimidinic (AP) sites, and decreased the activities of key enzymes in the BER pathway and superoxide dismutase (SOD), thereby escalating mtDNA damage. Meanwhile, H2O2 negatively regulated mitochondrial function by enlarging the openness of mitochondrial permeability transition pore, aggravating the consumption of oxygen, and reducing the respiratory control ratio of mitochondria and membrane potential. In contrast, NAC, working in conjunction with NO, substantially up-regulated gene expression of the BER pathway. It indicated that H2O2 treatment counteracted the NO-induced protection of mitochondria in cold-stored peaches. This study provides new insight for understanding the crosstalk of different signal molecules in plants.