LOCAL AND SYSTEMIC RESPONSES OF ANTIOXIDANTS TO TOBACCO MOSAIC-VIRUS INFECTION AND TO SALICYLIC-ACID IN TOBACCO - ROLE IN SYSTEMIC ACQUIRED-RESISTANCE

Citation
J. Fodor et al., LOCAL AND SYSTEMIC RESPONSES OF ANTIOXIDANTS TO TOBACCO MOSAIC-VIRUS INFECTION AND TO SALICYLIC-ACID IN TOBACCO - ROLE IN SYSTEMIC ACQUIRED-RESISTANCE, Plant physiology, 114(4), 1997, pp. 1443-1451
Citations number
63
Categorie Soggetti
Plant Sciences
Journal title
ISSN journal
00320889
Volume
114
Issue
4
Year of publication
1997
Pages
1443 - 1451
Database
ISI
SICI code
0032-0889(1997)114:4<1443:LASROA>2.0.ZU;2-M
Abstract
Changes in ascorbate and glutathione levels and in activities of ascor bate peroxidase, catalase, dehydroascorbate reductase (DHAR), glutathi one reductase (GR), glutathione S-transferase (CST), and superoxide di smutase (SOD) were investigated in tobacco mosaic virus (TMV)-inoculat ed lower leaves and in noninoculated upper leaves of Nicotiana tabacum L. cv Xanthi-nc. In separate experiments the effects of exogenous sal icylic acid (SA) were also studied. Symptom appearance after TMV inocu lation was preceded by a slight, transient decline of ascorbate peroxi dase, 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 declin ed 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, concom itantly with the development of systemic acquired resistance. From the six distinct SOD isoenzymes found in tobacco leaves, only the activit ies of Cu,Zn-SOD isoenzymes were affected by TMV. SA injection induced DHAR, GR, GST, and SOD activities. Catalase activities were not modif ied by TMV infection or SA treatment. It is supposed that stimulated a ntioxidative processes contribute to the suppression of necrotic sympt om development in leaves with systemic acquired resistance.