Abstract

Nitric oxide (NO) is a key molecule involved in many physiology processes. The effects of NO on alleviating arsenic-induced oxidative damage in tall fescue leaves were investigated. Arsenic (25 μM) treatment induced significantly accumulation of reactive oxygen species (ROS) and led to serious lipid peroxidation in tall fescue leaves and the application of 100 μM SNP before arsenic stress resulted in alleviated arsenic-induced electrolyte leakage and malondiadehyde (MDA) content in tall fescue leaves, the levels of hydrogen peroxide (H₂O₂) and superoxide radical (QUOTE  ) were reduced as well. Moreover, the activities of superoxide dismutase (SOD), catalase (CAT) and ascorbate peroxidase (APX) increased in tall fescue leaves in presence of SNP under arsenic stress. This pattern was reversed by application of NO scavenger, 2-(4-carboxy-2-phenyl)-4,4,5,5-tetramethy-limidazoline-1-oxyl-3-oxide (PTIO) before arsenic treatment. Pronounced increases in endogenous NO production was found in plants after exposure to arsenic stress. The results suggested that arsenic stress elevated endogenous NO level and that NO might act as a signaling molecule to enhance antioxidant enzyme activities, further protecting against injuries caused by arsenic toxicity.

Key words: Antioxidant enzymes, arsenic stress, nitric oxide, oxidative stress, tall fescue.

Abbreviation

NO, Nitric oxide; ROS, reactive oxygen species; MDA,malondiadehyde; SOD, superoxide dismutase; CAT, Catalase; APX, ascorbate peroxidase; POD, peroxidase; GR, glutathione reductase; PTIO, 2-(4-carboxy-2-phenyl)-4,4,5,5-tetramethylimidazoline--oxyl-3-oxide; REL, relative electrolyte leakage; As, arsenic; PPFD, photosynthetic photo flux density.