Heme oxygenase/carbon monoxide system participates in regulating wheat seed germination under osmotic stress involving the nitric oxide pathway.

To investigate the mechanism and signaling pathway of carbon monoxide (CO) and hematin in alleviating seed germination inhibition and lipid peroxidation, polyethylene glycol-6000 (PEG) was used to mimic osmotic stress in a series of experiments. The results showed that wheat seeds pretreated with a lower dose of PEG (12.5%) showed higher tolerance against osmotic stress as well as the up-regulation of heme oxygenase (HO, EC 1.14.99.3) and decreased lipid peroxidation during recuperation, compared to those with a higher dose of PEG (50%). Exposure of wheat seeds to 25% PEG, HO-1 inhibitor or specific scavenger of nitric oxide (NO) alone differentially led to seed germination inhibition. The PEG-induced inhibitory effects on seed germination were ameliorated by the HO-1 inducer hematin, CO or NO donor. Additionally, hematin was able to markedly boost the HO/CO system. However, the addition of the HO-1 inhibitor or the specific scavenger of NO not only reversed the protective effects conferred by hematin, but also blocked the up-regulation of HO/CO. In addition, hematin-driven NO production in wheat seeds under osmotic stress was confirmed. Based on these results, we conclude that the endogenous HO/CO signal system is required for the alleviation of osmotic stress-induced wheat seed germination inhibition and lipid peroxidation, which might have a possible interaction with NO.