Air Pollution, Photosynthesis and Forest Decline: Interactions and Consequences
285
the N02 concentration in the field. There is still confusion as to whether and
how nitrogen oxides affect plants directly at ambient concentrations in air
(d. Wellburn 1990). We conclude that the indirect toxic action of N02 via
ozone formation is much more important as a damaging factor than the
direct action.
14.5.3 The Fate of Ozone
Ozone and its highly reactive degradation products react with all plant
surfaces. However, it is doubtful whether reactions with epidermal structures
can cause damage comparable with that which ensues when ozone, after
penetrating open stomata, fails to be completely intercepted in the apoplasmic space of internal leaf tissues. Apoplasmic detoxification is the main
defense against ozone. On sunny days, peak ozone concentrations in air may
be 200ppb or more in Germany (Umweltbundesamt, Jahresbericht 1990). In
North America, concentrations up to 800ppb have been observed (Smith
1991). In spinach leaves, the redox state of apoplasmic ascorbate changed
from 90% reduced to 90% oxidized within 6 h of fumigation with 300 ppb
ozone (Luwe et al. 1993). Ascorbate regeneration could not keep pace with
oxidation which, however, accounted for only 10% or less of calculated
ozone fluxes into the leaves. Oxidized ascorbate could not be reduced in the
apoplasm. Rather, it was transferred into the cytosol and reduced there.
Cytosolic ascorbate was exported into the apoplasm, but transport was slow.
There is little doubt that apoplasmic antioxidants other than ascorbate
participated in apoplasmic ozone detoxification. Nevertheless, after about
12 h of fumigation with 300 ppb ozone, intracellular glutathione (but not
intracellular ascorbate) started to become oxidized. After 48 h of fumigation,
oxidation extended to intracellular ascorbate. Total ascorbate levels declined.
Simultaneously, necrotic leaf damage became visible. This shows that, at
300ppb ozone, apoplasmic anti oxidative defenses were overwhelmed.
Presumably, ozone reached the plasmalemma. This made ozonization of
unsaturated fatty acid residues and subsequent reactions inevitable. Urbach
et al. (1989) have calculated that only a smally percentage of the ozone
which reaches the plasmalemma actually manages to diffuse into the cytosol.
Most is intercepted within this biomembrane, damaging it by ozonization of
double bonds and subsequent reactions. This alters permeability properties.
At increased levels of ozone, intracellular ascorbate leaks into the apoplasm.
Whereas this may contribute to protection, apoplasmic levels of cations are
also increased, indicating a general loss of intracellular solutes. Even though,
by itself, this would not necessarily decrease the viability of affected cells,
tissues already suffering from mineral deficiency due to the loss of essential
minerals may be severely damaged.
It should be noted that, under field conditions, ozone is most unlikely to
reach concentrations in air which would affect intracellular organelles such
285
the N02 concentration in the field. There is still confusion as to whether and
how nitrogen oxides affect plants directly at ambient concentrations in air
(d. Wellburn 1990). We conclude that the indirect toxic action of N02 via
ozone formation is much more important as a damaging factor than the
direct action.
14.5.3 The Fate of Ozone
Ozone and its highly reactive degradation products react with all plant
surfaces. However, it is doubtful whether reactions with epidermal structures
can cause damage comparable with that which ensues when ozone, after
penetrating open stomata, fails to be completely intercepted in the apoplasmic space of internal leaf tissues. Apoplasmic detoxification is the main
defense against ozone. On sunny days, peak ozone concentrations in air may
be 200ppb or more in Germany (Umweltbundesamt, Jahresbericht 1990). In
North America, concentrations up to 800ppb have been observed (Smith
1991). In spinach leaves, the redox state of apoplasmic ascorbate changed
from 90% reduced to 90% oxidized within 6 h of fumigation with 300 ppb
ozone (Luwe et al. 1993). Ascorbate regeneration could not keep pace with
oxidation which, however, accounted for only 10% or less of calculated
ozone fluxes into the leaves. Oxidized ascorbate could not be reduced in the
apoplasm. Rather, it was transferred into the cytosol and reduced there.
Cytosolic ascorbate was exported into the apoplasm, but transport was slow.
There is little doubt that apoplasmic antioxidants other than ascorbate
participated in apoplasmic ozone detoxification. Nevertheless, after about
12 h of fumigation with 300 ppb ozone, intracellular glutathione (but not
intracellular ascorbate) started to become oxidized. After 48 h of fumigation,
oxidation extended to intracellular ascorbate. Total ascorbate levels declined.
Simultaneously, necrotic leaf damage became visible. This shows that, at
300ppb ozone, apoplasmic anti oxidative defenses were overwhelmed.
Presumably, ozone reached the plasmalemma. This made ozonization of
unsaturated fatty acid residues and subsequent reactions inevitable. Urbach
et al. (1989) have calculated that only a smally percentage of the ozone
which reaches the plasmalemma actually manages to diffuse into the cytosol.
Most is intercepted within this biomembrane, damaging it by ozonization of
double bonds and subsequent reactions. This alters permeability properties.
At increased levels of ozone, intracellular ascorbate leaks into the apoplasm.
Whereas this may contribute to protection, apoplasmic levels of cations are
also increased, indicating a general loss of intracellular solutes. Even though,
by itself, this would not necessarily decrease the viability of affected cells,
tissues already suffering from mineral deficiency due to the loss of essential
minerals may be severely damaged.
It should be noted that, under field conditions, ozone is most unlikely to
reach concentrations in air which would affect intracellular organelles such