title: Interactive role of nitric oxide and calcium chloride in enhancing tolerance to salt stress.
abstract: Nitric oxide (NO), a small diffusible, ubiquitous bioactive molecule, acts as prooxidant as well as antioxidant, and also regulates remarkable spectrum of plant cellular mechanisms. The present work was undertaken to investigate the role of nitric oxide donor sodium nitroprusside (SNP) and/or calcium chloride (CaCl(2)) in the tolerance of excised mustard leaves to salt stress. After 24h, salt stressed leaves treated with SNP and/or CaCl(2), showed an improvement in the activities of carbonic anhydrase (CA) and nitrate reductase (NR), and leaf chlorophyll (Chl) content, leaf relative water content (LRWC) and leaf ion concentration as compared with the leaves treated with NaCl only. Salinity stress caused a significant increase in H(2)O(2) content and membrane damage which is witnessed by enhanced levels of thiobarbituric acid reactive substances (TBARS) and electrolyte leakage. By contrast, such increases were blocked by the application of 0.2mM SNP and 10mM CaCl(2) to salt stressed leaves. Application of SNP and/or CaCl(2) alleviated NaCl stress by enhancing the activities of antioxidative enzymes viz. superoxide dismutase (SOD), catalase (CAT), peroxidase (POX), ascorbate peroxidase (APX) and glutathione reductase (GR) and by enhancing proline (Pro) and glycinebetaine (GB) accumulation with a concomitant decrease in H(2)O(2) content, TBARS and electrolyte leakage, which is manifested in the tolerance of plants to salinity stress. Moreover, application of SNP with CaCl(2) was more effective to reduce the detrimental effects of NaCl stress on excised mustard leaves. In addition to this, ameliorating effect of SNP was not effective in presence of NO scavenger cPTIO [2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide]. To put all these in a nut shell, the results advocate that SNP in association with CaCl(2) plays a role in enhancing the tolerance of plants to salt stress by improving antioxidative defence system, osmolyte accumulation and ionic homeostasis.
authors.affiliation: Department of Biology, Faculty of Science, University of Tabuk, Tabuk 71491, Saudi Arabia. nasirmn4@gmail.com
authors.forename: M Nasir
authors.initials: MN
authors.lastname: Khan
authors.forename: Manzer H
authors.initials: MH
authors.lastname: Siddiqui
authors.forename: Firoz
authors.initials: F
authors.lastname: Mohammad
authors.forename: M
authors.initials: M
authors.lastname: Naeem
mesh_terms: D000975:Antioxidants / Q000494:pharmacology; D001565:Benzoates / Q000378:metabolism / Q000494:pharmacology; D002122:Calcium Chloride / Q000378:metabolism*; D002374:Catalase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D007093:Imidazoles / Q000378:metabolism / Q000494:pharmacology; D015227:Lipid Peroxidation; D009569:Nitric Oxide / Q000378:metabolism*; D009599:Nitroprusside / Q000494:pharmacology; D010544:Peroxidases / Q000378:metabolism; D018515:Plant Leaves / Q000187:drug effects*; D012965:Sodium Chloride / Q000494:pharmacology*; D013312:Stress, Physiological; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D000975:Antioxidants; D001565:Benzoates; D007093:Imidazoles; D017392:Thiobarbituric Acid Reactive Substances; C079393:1,3-dihydroxy-4,4,5,5-tetramethyl-2-(4-carboxyphenyl)tetrahydroimidazole; D009599:Nitroprusside; D009569:Nitric Oxide; D012965:Sodium Chloride; D010544:Peroxidases; D002374:Catalase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D002122:Calcium Chloride