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Local and systemic responses to antioxidants to tobacco mosaic virus infection and to salicylic acid to tobacco. Role in systemic acquired resistance

Fodor, J., Gullner, G., Adam, A.L., Barna, B., Komives, T., Kiraly, Z.
Plant physiology 1997 v.114 no.4 pp. 1443-1451
Nicotiana tabacum, Tobacco mosaic virus, leaves, pathogenicity, necrosis, disease resistance, antioxidants, ascorbic acid, glutathione, quantitative analysis, peroxidases, catalase, dehydroascorbic acid, oxidoreductases, glutathione reductase (NADPH), glutathione transferase, superoxide dismutase, enzyme activity, isozymes, salicylic acid, dose response, chemical constituents of plants
Changes in ascorbate and glutathione levels and in activitiesof ascorbate peroxidase, catalase, dehydroascorbate reductase (DHAR), glutathione reductase (GR), glutathione S-transferase (GST), and superoxide dismutase (SOD) were investigated in tobacco mosaic virus (TMV)-inoculated lower leaves and in noninoculated upper leaves of Nicotiana tabacum L. cv Xanthi-nc. In separate experiments the effects of exogenous salicylic acid (SA) were also studied. Symptom appearance after TMV inoculation was preceded by a slight, transient decline of ascorbate peroxidase, GR, GST, and SOD activities in the inoculated lower leaves, but after the onset of necrosis these activities and the glutathione level substantially increased. Ascorbic acid level and DHAR activity declined and dehydroascorbate accumulated in the inoculated leaves. In upper leaves, the glutathione level and the activities of GR, GST, and SOD increased 10 to 14 d after TMV inoculation of the lower leaves, concomitantly with the development of systemic acquired resistance. From the six distinct SOD isoenzymes found in tobacco leaves, only the activities of Cu,Zn-SOD isoenzymes were affected by TMV. SA injection induced DHAR, GR, GST, and SOD activities. Catalase activities were not modified by TMV infection or SA treatment. It is supposed that stimulated antioxidative processes contribute to the suppression of necrotic symptom development in leaves with systemic acquired resistance.