Protective effect of nitric oxide on light-induced oxidative damage in leaves of tall fescue.

Nitric oxide (NO) is an important signaling molecule involved in many physiological processes. In this study, the effect of NO on oxidative damage caused by high levels of light was investigated in leaves of two varieties of tall fescue (Arid3 and Houndog5). Leaves of Houndog5 were more susceptible to high-light stress than Arid3 leaves. Pretreatment of these leaves with NO donor sodium nitroprusside (SNP), prior to exposure to high-light stress, resulted in reduced light-induced electrolyte leakage and reduced contents of malondialdehyde, hydrogen peroxide (H(2)O(2)) and superoxide radicals (O(2)(*-)). The activities of superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX) and glutathione reductase (GR) increased in both varieties in the presence of SNP under high-light stress, but lipoxygenase (LOX) activity was inhibited. These responses could be reversed by pretreatment with the NO scavenger 2-(4-carboxy-2-phenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (PTIO). A pronounced increase in nitric oxide synthase (NOS) activity and NO release was found in light-tolerant Arid3 plants after exposure to high-light stress, while only a small increase was observed in more sensitive Houndog5. Pretreatment with the NOS inhibitor N(omega)-nitro-l-arginine (LNNA) resulted in increased oxidative damage under high-light stress, with more injuries occurring in Arid3 than Houndog5. These results suggest that high-light stress induced increased NOS activity leading to elevated NO. This NO might act as a signaling molecule triggering enhanced activities of antioxidant enzymes, further protecting against injuries caused by high intensity light. This protective mechanism was found to more efficiently acclimate light-tolerant Arid3 than light-sensitive Houndog5.