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Ozone‐induced oxidative burst in the ozone biomonitor plant, tobacco Bel W3
Author(s) -
Schraudner Martina,
Moeder Wolfgang,
Wiese Cosima,
Camp Wim Van,
Inzé Dirk,
Langebartels Christian,
Sandermann Heinrich
Publication year - 1998
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1046/j.1365-313x.1998.00294.x
Subject(s) - ozone , superoxide , reactive oxygen species , apoplast , programmed cell death , chemistry , nicotiana tabacum , respiratory burst , hypersensitive response , microbiology and biotechnology , horticulture , biochemistry , biology , cell wall , apoptosis , gene , enzyme , organic chemistry
Summary Localized cell death is a common feature of ozone phytotoxicity and is generally thought to be initiated by the strong oxidant ozone itself as well as by ozone‐derived reactive oxygen intermediates (ROIs). Here we report that ozone (150 nl l –1 , 5 h) elicits cellular ROI production in the ozone‐sensitive tobacco cv. Bel W3, but not in the tolerant cv. Bel B. Both cultivars exhibited a transient first maximum of apoplastic ROI accumulation followed by a comparable induction of glutathione peroxidase transcript levels. During postcultivation in pollutant‐free air, a second and sustained peak of apoplastic ROI accumulation was detected only in cv. Bel W3. Histochemical staining revealed a spot‐like accumulation of H 2 O 2 and, to a lesser extent, of superoxide anion radicals in this cultivar. The H 2 O 2 spots (‘burst initiation sites’) occurred mainly in the vicinity of leaf veins and correlated in number and distribution with discrete sites of local cell death and with visible symptoms that evolved between 15 and 72 h. The results indicate that ozone effects are amplified in the sensitive tobacco cv. Bel W3 by an oxidative burst which participates in the generation of hypersensitive cell death‐like lesions.