Figure 9.

Mechanisms underlying nitric oxide (NO) and hydrogen sulfide (H₂S) crosstalk evoked thermotolerance in maize seedlings. Nitric oxide (NO) donor sodium nitroprusside (SNP) could trigger hydrogen sulfide (H₂S) signaling by up-regulated LCD1 expression and L-cysteine desulfhydrase (LCD) and D-cysteine desulfhydrase (DCD) activities. Then, the activity of the ROS-scavenging system, including enzymatic (ascorbate peroxidase, APX; dehydroascorbate reductase, DHAR; monodehydroascorbate reductase, MDHAR;glutathione reductase, GR; catalase, CAT; and superoxide dismutase, SOD) and non-enzymatic (ascorbic acid, AsA; glutathione, GSH; flavonoids, FLA; carotenoids, CAR; and total phenols, TP) antioxidants, was enhance by SNP, which in turn increased survival rate (SR) and tissue viability, decreased electrolyte leakage (EL), malondialdehyde (MDA), superoxide radical (O₂ ^.-), and hydrogen peroxide (H₂O₂) levels, thus evoking thermotolerance of maize seedlings. Also, the SNP-evoked thermotolerance could be weakened by 2-(4-carboxyphenyl)-4,4,5,5- tetrameth- ylimidazoline-1-oxyl-3-oxide (cPTIO), DL-propargylglycine (PGA), and hypotaurine (HT) alone, indicating that ROS-scavenging system plays a key role in the SNP-evoked thermotolerance in maize seedlings. The arrows (↑), (↓), and (⊥) denote increase, decrease, and inhibition, respectively.