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.
Highlights
Arsenic (As) is one of the five kinds of toxic heavy metals and it is distributed widely in natural environment
The results showed that supplementation of these residual products had little effect on electrolyte leakage in tall fescue leaves under arsenic stress (Figure 1B)
Our results indicated that tall fescue leaves exhibited increases in the activities of antioxidant enzymes (SOD, CAT and ascorbate peroxidase (APX)) both 4 and 8 days after arsenic treatment (Figures 4A - C)
Summary
Arsenic (As) is one of the five kinds of toxic heavy metals and it is distributed widely in natural environment. Stresses (drought, heat, salinity, UV-B radiation and heavy metals) generation of reactive oxygen species (ROS: H2O2, hydrogen peroxide; , superoxide radical, HO, hydroxyl radical; O21, singlet oxygen) increased and resulted in oxidative stress in plant cells (Mittler, 2002; Schützendübel and Polle, 2002; Apel and Hirt, 2004). If these ROS are not removed immediately, it can cause damage to the cell membrane and even death (Gratao et al, 2005). To avoid ROS induced cellular injury, plants employ various antioxidative enzymes such as superoxide dismutase (SOD: EC 1.15.1.1), catalase (CAT: EC 1.11.1.6), peroxidase (POD: EC 1.11.1.7), ascorbate peroxidase (APX: EC 1.11.1.11), glutathione reductase (GR: EC 1.6.4.2) (Apel and Hirt, 2004)
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