Effects of ozone on the carbon metabolism of forest trees

Chronic long-term exposure to near-ambient concentrations of ozone could co ntribute 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 s ymptoms of damage. Photosynthesis is impaired whereas respiration is increa sed. The activity and quantity of Rubisco and Rubisco activase are diminish ed 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 impre ssive event is the huge increase in activity of phosphoenolpyruvate carboxy lase linked to a stimulation of the enzyme biosynthesis. Therefore, the hig h 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 c hanges in cellular metabolism are directed towards repair and maintenance o f the cell structure. In this respect, a general increase in the phenylprop anoid metabolism is also observed with the production of more phenolic comp ounds and a stimulation of the lignin biosynthetic pathway through the acti vation of several enzymes (phenylalanine ammonia lyase, cinnamyl alcohol de hydrogenase, etc.). The mechanism of ozone action however still remains to be elucidated. Ozone causes an oxidative stress producing reactive oxygen s pecies, which are the probable source for signal chains with messenger mole cules such as jasmonic acid, salicylic acid and ethylene. The problem remai ns of the existence of a specific series of events starting from ozone pene trating through the stomata to the repression/stimulation of gene transcrip tion in foliar cells. (C) 2001 Editions scientifiques et medicales Elsevier SAS.