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Subcellular localization of ozone‐induced hydrogen peroxide production in birch (Betula pendula) leaf cells
Author(s) -
Pellinen Riikka,
Palva Tapio,
Kangasjärvi Jaakko
Publication year - 1999
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.1999.00613.x
Subject(s) - reactive oxygen species , microbiology and biotechnology , mitochondrion , betula pendula , oxidative stress , chemistry , peroxisome , mitochondrial ros , superoxide , hydrogen peroxide , cytoplasm , biochemistry , biology , botany , enzyme , gene
Summary The atmospheric air pollutant ozone (O 3 ) is one of the environmental stresses that induce formation of reactive oxygen species (ROS) in plants. Previously, the toxicity of O 3 has been believed to be a result of ROS formation from O 3 ‐degradation. Recently, however, it has been shown that O 3 induces active ROS production, which suggests that O 3 ‐responses may be mechanistically similar to pathogen‐induced responses and that O 3 ‐damage could be a result of deleterious firing by the ROS of pathways normally associated with the HR. The subcellular localization of O 3 ‐induced H 2 O 2 production was studied in birch ( Betula pendula ). O 3 induced H 2 O 2 accumulation first on the plasma membrane and cell wall. Experiments with inhibitors of possible sources for H 2 O 2 in the cell wall suggested that both NADPH‐dependent superoxide synthase and the cell wall peroxidases are involved in this H 2 O 2 production. The H 2 O 2 production continued in the cytoplasm, mitochondria and peroxisomes when the O 3 ‐exposure was over, but not in chloroplasts. The timing of mitochondrial H 2 O 2 accumulation coincided with the first symptoms of visible damage and, at the same time, the mitochondria showed disintegration of the matrix. These responses may not be directly connected with defense against oxidative stress, but may rather indicate changes in oxidative balance within the cells that affect mitochondrial metabolism and the homeostasis of the whole cell, possibly leading into induction of programmed cell death.