When leaves of plants are subjected to stress, a frequent response is the acceleration of the senescence process. Fluckiger et al. (1979) observed that foliage of many trees and shrubs exhibited accelerated leaf abscission when the plants were grown in containers along a motorway. While the causal agent(s) inducing accelerated senescence was not defined in this study, the response is an indication of the role the atmosphere plays in altering leaf longevity. Occasional reports suggest that sulfur dioxide exposure can lead to more rapid aging of foliage (Kargiolaki et al., 1991) and there is an extensive literature describing ozone (O3) induction of premature or accelerated leaf senescence (Mikkelsen and Heide-J0rgensen, 1996; Ojanpera et al., 1998; Pell et al., 1997; Reich and Lassoie, 1985), as will be discussed below.

Ozone was first discovered as an air pollutant capable of causing injury to foliage in the 1950s (Richards et al., 1958). While higher concentrations of the gas readily lead to regions of leaf necrosis, chronic exposures to relatively low concentrations of the gas have become associated with signs of accelerated leaf senescence (Pell et al., 1997). In this chapter we will explore the evidence that O3 induces accelerated leaf senescence, the mechanism by which this induction might occur, and the implications to the whole plant.

Ozone enters the leaf almost exclusively through stomates (Laisk et al., 1989) and is either scavenged in the apoplastic fluid or begins to penetrate the cells. Since O3 is so reactive, it is thought that virtually no gas penetrates the cell membrane (Laisk et al., 1989). Rather, reactions either within the wall or membrane are likely to generate reactive oxygen species (ROS) with high oxidizing potential, e.g. OH°, RO°, O2-, or H2O2 (Kangasjarvi et al., 1994; Ranieri et al., 1999). While most of the ROS are highly reactive and will not persist, H2O2 is a more stable byproduct capable of movement throughout the cell (Levine et al., 1994). The ability of cells to withstand elevated levels of O3-generated oxidative stress will depend upon the capacity of the cell to scavenge ROS (Kangasjarvi et al., 1994; Pell etal., 1999).

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