title: Redox homeostasis, antioxidant defense, and methylglyoxal detoxification as markers for salt tolerance in Pokkali rice.
abstract: To identify biochemical markers for salt tolerance, two contrasting cultivars of rice (Oryza sativa L.) differing in salt tolerance were analyzed for various parameters. Pokkali, a salt-tolerant cultivar, showed considerably lower level of H(2)O(2) as compared to IR64, a sensitive cultivar, and such a physiology may be ascribed to the higher activity of enzymes in Pokkali, which either directly or indirectly are involved in the detoxification of H(2)O(2). Enzyme activities and the isoenzyme pattern of antioxidant enzymes also showed higher activity of different types and forms in Pokkali as compared to IR64, suggesting that Pokkali possesses a more efficient antioxidant defense system to cope up with salt-induced oxidative stress. Further, Pokkali exhibited a higher GSH/GSSG ratio along with a higher ratio of reduced ascorbate/oxidized ascorbate as compared to IR64 under NaCl stress. In addition, the activity of methylglyoxal detoxification system (glyoxalase I and II) was significantly higher in Pokkali as compared to IR64. As reduced glutathione is involved in the ascorbate-glutathione pathway as well as in the methylglyoxal detoxification pathway, it may be a point of interaction between these two. Our results suggest that both ascorbate and glutathione homeostasis, modulated also via glyoxalase enzymes, can be considered as biomarkers for salt tolerance in Pokkali rice. In addition, status of reactive oxygen species and oxidative DNA damage can serve as a quick and sensitive biomarker for screening against salt and other abiotic stresses in crop plants.
authors.affiliation: Plant Molecular Biology, International Centre for Genetic Engineering and Biotechnology (ICGEB), Aruna Asaf Ali Marg, New Delhi, 110 067, India.
authors.forename: Hattem
authors.initials: H
authors.lastname: El-Shabrawi
authors.forename: Bhumesh
authors.initials: B
authors.lastname: Kumar
authors.forename: Tanushri
authors.initials: T
authors.lastname: Kaul
authors.forename: Malireddy K
authors.initials: MK
authors.lastname: Reddy
authors.forename: Sneh L
authors.initials: SL
authors.lastname: Singla-Pareek
authors.forename: Sudhir K
authors.initials: SK
authors.lastname: Sopory
mesh_terms: D000975:Antioxidants / Q000378:metabolism*; D001205:Ascorbic Acid / Q000378:metabolism; D015415:Biomarkers / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D004249:DNA Damage; D005978:Glutathione / Q000378:metabolism; D019803:Glutathione Disulfide / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D006706:Homeostasis; D006861:Hydrogen Peroxide / Q000378:metabolism; D007527:Isoenzymes / Q000378:metabolism; D007791:Lactoylglutathione Lyase / Q000378:metabolism; D012275:Oryza / Q000502:physiology*; D016877:Oxidants / Q000378:metabolism; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D010940:Plant Proteins / Q000378:metabolism*; D011392:Proline / Q000378:metabolism; D011765:Pyruvaldehyde / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism; D055049:Salt Tolerance / Q000502:physiology*; D012965:Sodium Chloride / Q000378:metabolism; D013869:Thiolester Hydrolases / Q000378:metabolism; D000099301:Hydroxyacylglutathione Hydrolase
chemical_list: D000975:Antioxidants; D001205:Ascorbic Acid; D015415:Biomarkers; D002374:Catalase; D005978:Glutathione; D019803:Glutathione Disulfide; D005979:Glutathione Peroxidase; D006861:Hydrogen Peroxide; D007527:Isoenzymes; D007791:Lactoylglutathione Lyase; D016877:Oxidants; D010940:Plant Proteins; D011392:Proline; D011765:Pyruvaldehyde; D017382:Reactive Oxygen Species; D012965:Sodium Chloride; D013869:Thiolester Hydrolases; D000099301:Hydroxyacylglutathione Hydrolase