ANTIOXIDANT RESPONSES OF RICE SEEDLINGS TO SALINITY STRESS

Citation
Ml. Dionisiosese et S. Tobita, ANTIOXIDANT RESPONSES OF RICE SEEDLINGS TO SALINITY STRESS, PLANT SCI, 135(1), 1998, pp. 1-9
Citations number
33
Categorie Soggetti
Plant Sciences
Journal title
PLANT SCIENCE
ISSN journal
01689452 → ACNP
Volume
135
Issue
1
Year of publication
1998
Pages
1 - 9
Database
ISI
SICI code
0168-9452(1998)135:1<1:ARORST>2.0.ZU;2-3
Abstract
The possible involvement of activated oxygen species in the mechanism of damage by NaCl stress was studied in leaves of four varieties of ri ce (Oryza sativa L.) exhibiting different sensitivities to NaCl. The 3 -week-old rice seedlings were subjected to 0, 6 and 12 dS m(-1) salini ty levels for 1-week after which differences in antioxidant capacities and possible correlation, growth rate and Na+ uptake of the leaves we re analyzed. High salinity treatment caused a decrease in growth rate in all the varieties tested except Pokkali. The salt-sensitive varieti es, Hitomebore and IR28, exhibited a decrease in superoxide dismutase activity and an increase in peroxidase activity under high salinizatio n. These varieties also exhibited increase in lipid peroxidation and e lectrolyte leakage as well as higher Na+ accumulation in the leaves un der salt stress. The salt-tolerant variety Pokkali however, showed onl y slight increase and decrease in superoxide dismutase and peroxidase activity, respectively, and virtually unchanged lipid peroxidation, el ectrolyte leakage and Na+ accumulation upon salinization. On the other hand, the putative salt-tolerant Bankat variety, which showed a sligh t stimulation in growth rate similar to Pokkali at moderate salinity l evel, exhibited Na+ accumulation and symptoms of oxidative damage duri ng salt stress similar to the salt-sensitive varieties rather than the salt-tolerant one. These results indicate that free radical-mediated damage of membrane may play an important role in the cellular toxicity of NaCl in rice seedlings and that salt-tolerant varieties exhibit pr otection mechanism against increased radical production by maintaining the specific activity of antioxidant enzymes. (C) 1998 Elsevier Scien ce Ireland Ltd. All rights reserved.