Subcellular localization of ozone-induced hydrogen peroxide production in birch (Betula pendula) leaf cells
Article first published online: 1 MAY 2002
The Plant Journal
Volume 20, Issue 3, pages 349–356, November 1999
How to Cite
Pellinen, R., Palva, T. and Kangasjärvi, J. (1999), Subcellular localization of ozone-induced hydrogen peroxide production in birch (Betula pendula) leaf cells. The Plant Journal, 20: 349–356. doi: 10.1046/j.1365-313X.1999.00613.x
- Issue published online: 1 MAY 2002
- Article first published online: 1 MAY 2002
- Received 23 June 1999; revised 24 September 1999; accepted 27 September 1999.
The atmospheric air pollutant ozone (O3) is one of the environmental stresses that induce formation of reactive oxygen species (ROS) in plants. Previously, the toxicity of O3 has been believed to be a result of ROS formation from O3-degradation. Recently, however, it has been shown that O3 induces active ROS production, which suggests that O3-responses may be mechanistically similar to pathogen-induced responses and that O3-damage could be a result of deleterious firing by the ROS of pathways normally associated with the HR. The subcellular localization of O3-induced H2O2 production was studied in birch (Betula pendula). O3 induced H2O2 accumulation first on the plasma membrane and cell wall. Experiments with inhibitors of possible sources for H2O2 in the cell wall suggested that both NADPH-dependent superoxide synthase and the cell wall peroxidases are involved in this H2O2 production. The H2O2 production continued in the cytoplasm, mitochondria and peroxisomes when the O3-exposure was over, but not in chloroplasts. The timing of mitochondrial H2O2 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.