title: Abscisic acid-regulated responses of aba2-1 under osmotic stress: the abscisic acid-inducible antioxidant defence system and reactive oxygen species production.
abstract: We investigated the interaction among abscisic acid (ABA), reactive oxygen species (ROS) and antioxidant defence system in the transduction of osmotic stress signalling using Arabidopsis thaliana WT (Columbia ecotype, WT) and an ABA-deficient mutant (aba2-1). For this, 50 μm ABA and osmotic stress, induced with 40% (w/v) polyethylene glycol (PEG8000; -0.7 MPa), were applied to WT and aba2-1 for 6, 12 or 24 h. Time course analysis was undertaken for determination of total/isoenzyme activity of the antioxidant enzymes, superoxide dismutase (SOD; EC 1.15.1.1), catalase (CAT; EC 1.11.1.6), ascorbate peroxidase (APX; EC 1.11.1.11), NADPH oxidase (NOX; EC 1.6.3.1) activity; scavenging activity of the hydroxyl radical (OH˙), hydrogen peroxide (H(2) O(2) ); endogenous ABA and malondialdehyde (MDA). The highest H(2) O(2) and MDA content was found in PEG-treated groups of both genotypes, but with more in aba2-1. ABA treatment under stress reduced the accumulation of H(2) O(2) and MDA, while it promoted activity of SOD, CAT and APX. APX activity was higher than CAT activity in ABA-treated WT and aba2-1, indicating a protective role of APX rather than CAT during osmotic stress-induced oxidative damage. Treatment with ABA also significantly induced increased NOX activity. Oxidative damage was lower in ABA-treated seedlings of both genotypes, which was associated with greater activity of SOD (Mn-SOD1 and 2 and Fe-SOD isoenzymes), CAT and APX in these seedlings after 24 h of stress. These results suggest that osmotic stress effects were overcome by ABA treatment because of increased SOD, CAT, APX and NOX.
authors.affiliation: Department of Biology, Faculty of Science, Ege University, Bornova, Izmir, Turkey.
authors.forename: C
authors.initials: C
authors.lastname: Ozfidan
authors.forename: I
authors.initials: I
authors.lastname: Turkan
authors.forename: A H
authors.initials: AH
authors.lastname: Sekmen
authors.forename: B
authors.initials: B
authors.lastname: Seckin
mesh_terms: D000040:Abscisic Acid / Q000378:metabolism / Q000494:pharmacology*; D000975:Antioxidants / Q000378:metabolism*; D017360:Arabidopsis / Q000187:drug effects* / Q000201:enzymology / Q000276:immunology / Q000502:physiology*; D060387:Ascorbate Peroxidases / Q000187:drug effects / Q000378:metabolism; D002374:Catalase / Q000187:drug effects / Q000378:metabolism; D005838:Genotype; D006861:Hydrogen Peroxide / Q000378:metabolism; D017665:Hydroxyl Radical / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008315:Malondialdehyde / Q000378:metabolism; D009154:Mutation; D019255:NADPH Oxidases / Q000187:drug effects / Q000378:metabolism; D009995:Osmosis / Q000187:drug effects*; D018384:Oxidative Stress / Q000187:drug effects; D018515:Plant Leaves / Q000187:drug effects / Q000276:immunology / Q000502:physiology; D011092:Polyethylene Glycols / Q000494:pharmacology; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects; D013312:Stress, Physiological / Q000187:drug effects; D013482:Superoxide Dismutase / Q000187:drug effects / Q000378:metabolism
chemical_list: D000975:Antioxidants; D017382:Reactive Oxygen Species; D017665:Hydroxyl Radical; D011092:Polyethylene Glycols; D008315:Malondialdehyde; D000040:Abscisic Acid; D006861:Hydrogen Peroxide; D060387:Ascorbate Peroxidases; D002374:Catalase; D013482:Superoxide Dismutase; D019255:NADPH Oxidases