Differential stress responses of antioxidative systems to drought in pendunculate oak (Quercus robur) and maritime pine (Pinus pinaster) grown under high CO(2) concentrations.
Maritime pine (Pinus pinaster), a drought-avoiding species, contained 2--4-fold lower activities of superoxide dismutase, ascorbate peroxidase, catalase, dehydroascorbate reductase, and glutathione reductase than pendunculate oak (Quercus robur), a drought-tolerant species. The levels of ascorbate, monodehydroascorbate radical reductase activity, and glutathione in pine needles were similar to those in oak leaves. In both species the development of drought stress, characterized by decreasing predawn water potentials, caused gradual reductions in antioxidant protection, increased lipid peroxidation, increased oxidation of ascorbate and glutathione and in pine also significant loss in soluble proteins and carotenoids. These results support the idea that increased drought-tolerance in oak as compared with pine is related to increased biochemical protection at the tissue level. To test the hypothesis that elevated CO(2) ameliorated drought-induced injury, young oak and pine trees acclimated to high CO(2) were subjected to drought stress. Analysis of plots of enzymatic activities and metabolites against predawn water potentials revealed that the drought stress-induced decreases in antioxidant protection and increases in lipid peroxidation were dampened at high CO(2). In pine, protein and pigment degradation were also slowed down. At high CO(2), superoxide dismutase activities increased transiently in drought-stressed trees, but collapsed in pine faster than in oak. These observations suggest that the alleviation of drought-induced injury under elevated CO(2) is related to a higher stability of antioxidative enzymes and an increased responsiveness of SOD to stressful conditions. This ameliorating mechanism existed independently from the effects of elevated CO(2) on plant water relations and is limited within a species-specific metabolic window.
Schwanz
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Albert-Ludwigs-Universität Freiburg, Institut für Forstbotanik und Baumphysiologie, Am Flughafen 17, D-79085 Freiburg, Germany.
Polle
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D000975:Antioxidants / Q000378:metabolism*; D060387:Ascorbate Peroxidases; D002245:Carbon Dioxide / Q000008:administration & dosage / Q000494:pharmacology*; D002338:Carotenoids / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D002734:Chlorophyll / Q000378:metabolism; D032462:Cycadopsida / Q000187:drug effects / Q000378:metabolism* / Q000502:physiology; D004190:Disasters; D005978:Glutathione / Q000032:analysis / Q000378:metabolism; D016014:Linear Models; D015227:Lipid Peroxidation / Q000502:physiology; D019684:Magnoliopsida / Q000187:drug effects / Q000378:metabolism* / Q000502:physiology; D010084:Oxidation-Reduction; D010088:Oxidoreductases / Q000378:metabolism; D010544:Peroxidases / Q000378:metabolism; D018515:Plant Leaves / Q000187:drug effects / Q000254:growth & development / Q000502:physiology; D013482:Superoxide Dismutase / Q000378:metabolism; D014867:Water / Q000502:physiology*
D000975:Antioxidants; D014867:Water; D002734:Chlorophyll; D002245:Carbon Dioxide; D002338:Carotenoids; D010088:Oxidoreductases; D010544:Peroxidases; D060387:Ascorbate Peroxidases; D002374:Catalase; D013482:Superoxide Dismutase; C020666:glutathione dehydrogenase (ascorbate); D005978:Glutathione