Effects of ozone on the carbon metabolism of forest trees

Chronic long-term exposure to near-ambient concentrations of ozone could contribute to forest decline in several regions of the world, in combination with other biotic and abiotic factors. It is generally admitted that, under ozone stress, biochemical events occur before any development of visible symptoms of damage. Photosynthesis is impaired whereas respiration is increased. The activity and quantity of Rubisco and Rubisco activase are diminished as well as the transcription of the proteins. Concomitantly, there is a general increase in the functioning of the catabolic pathways (glycolysis, pentose phosphate pathway). The mitochondrial respiration is also activated with an increased transcription of the alternative oxidase. The most impressive event is the huge increase in activity of phosphoenolpyruvate carboxylase linked to a stimulation of the enzyme biosynthesis. Therefore, the high ratio between the two carboxylases, which reaches about 25 in ozone-free air, falls to about 2 under ozone fumigation. There is also an increase in the detoxifying processes (chloroplastic superoxidase isoform). All these changes in cellular metabolism are directed towards repair and maintenance of the cell structure. In this respect, a general increase in the phenylpropanoid metabolism is also observed with the production of more phenolic compounds and a stimulation of the lignin biosynthetic pathway through the activation of several enzymes (phenylalanine ammonia lyase, cinnamyl alcohol dehydrogenase, etc.). The mechanism of ozone action however still remains to be elucidated. Ozone causes an oxidative stress producing reactive oxygen species, which are the probable source for signal chains with messenger molecules such as jasmonic acid, salicylic acid and ethylene. The problem remains of the existence of a specific series of events starting from ozone penetrating through the stomata to the repression/stimulation of gene transcription in foliar cells. (C) 2001 Editions scientifiques et medicales Elsevier SAS.