Nitric oxide mediates abscisic acid induced light-tolerance in leaves of tall fescue under high-light stress

- High-light stress increases oxidative damage in tall fescue leaves.
- NO acts as signaling molecule inducing activities of ROS-scavenging enzymes.
- NO mediates ABA induced light-tolerance in leaves under high-light stress.
- NO might operate downstream of ABA.

Abscisic acid (ABA) and nitric oxide (NO) are both extremely important signaling molecules involved in many physiological processes. In this study, the effect of ABA and NO on oxidative damage caused by high levels of light was investigated in leaves of two varieties of tall fescue (Arid3 and Houndog5). Pretreatment of these leaves with exogenous ABA, prior to exposure to high-light (HL) stress, resulted in reduced light-induced ion leakage and reduced content of malondialdehyde (MDA), hydrogen peroxide (H2O2) and superoxide radical. The activities of superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX) and glutathione reductase (GR) increased in both varieties in the presence of ABA under HL stress. These responses could be reversed by pretreatment with fluridone (the ABA biosynthesis inhibitor). A pronounced increase in nitric oxide synthase (NOS)-like activity and NO release by exogenous ABA treatment was found in light-tolerant Arid3 plants after exposure to high light, while only a small increase was observed in more sensitive Houndog5. Furthermore, inhibition of NO accumulation by 2-(4-carboxy-2-phenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (PTIO) or Nω-nitro-l-arginine (LNNA) blocked the protective effect of exogenous ABA, whereas inhibition of ABA by fluridone had no influence on the protective effect of NO. These results suggested that NO was involved in the ABA-induced activities of antioxidant enzymes, further protecting against injuries caused by high intensity light.