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U. Heber et al.
as chloroplasts directly. It damages cells before it actually reaches the
chloroplasts. Photosynthesis of intact chloroplasts which are suspended in
an isotonic sorbitol medium remains uninhibited when the suspension is
exposed to ozone at concentrations which kill leaves (Urbach, pers. comm.).
The simple explanation is that ozone reacts with constitutents of the medium
before it can damage the chloroplasts, even though these are highly sensitive
to oxidants.
Nevertheless, even low concentrations of ozone in air have been observed
to decrease the productivity of birch trees (Matyssek et al. 1992). Apparently,
effects of ozone on photosynthesis are of indirect nature. If forest trees,
where leaves or needles are exposed' to air polluted with ozone during
their life span, do not possess antioxidative defenses which are superior to
those of birch trees (or of spinach), ozone will contribute to forest decline.
Sandermann et al. (1989) summarized subacute effects of ozone on the
metabolism of conifers. He observed that latent damage after fumigation
with ozone found expression only in the following vegetation period
("memory effect").
14.5.4 The Fate of S02
Like N02, S02 may be hydrated already in the aqueous phase of the
apoplasm. Sulfite anions of the resultant sulfurous acid can be oxidized to
sulfite radicals by the oxidized phenolics which are formed in the apoplasm
by the reaction of peroxidase with hydrogen peroxide and apoplasmic
phenolics (Pfanz et al. 1990; Takahama et al. 1993). The radicals are readily
reduced by apoplasmic ascorbate. However, since little or no oxidation of
apoplasmic ascorbate has been observed during fumigation of leaves with
high concentrations of S02 (Takahama et al. 1993), a radical chain oxidation
of sulfite to sulfate seems to be prevented in the apoplasm by ascorbate
(but see Pfanz and Oppmann 1991). Irrespective of what happens in the
apoplasm, the inhibition of photosynthesis observed 1 or 2 min after onset of
fumigation of leaves with high concentrations of S02 (2 to 6ppm, VeljovicJovanovic et al. 1993) shows that S02 and its hydration products rapidly
enter the cytoplasm. Sulfurous acid decreases the cytoplasmic pH, stimulating
the cytoplasmic pH-stat mechanisms which counter acidification (Pfanz et al.
1987; Pfanz and Heber 1989; Pfanz and Heber et al. 1989b; Yin 1990;
Veljovic-Jovanovic et al. 1993). The phosphate translocator of the chloroplast envelope catalyzes not only exchange of phosphate and phosphate
esters between cytosol and chloroplast stroma, but also permits transfer of
sulfite and sulfate (Hampp and Ziegler 1977; Hampp et al. 1980). In the
chloroplasts, sulfite is detoxified either by reduction to the sulfide level or by
oxidation to sulfate (Dittrich et al. 1992). Effective reduction which leads to
the amino acid cysteine depends on the presence of O-acetylserine. Chloroplastic radical scavengers prevent the fast radical chain oxidation of sulfite to
U. Heber et al.
as chloroplasts directly. It damages cells before it actually reaches the
chloroplasts. Photosynthesis of intact chloroplasts which are suspended in
an isotonic sorbitol medium remains uninhibited when the suspension is
exposed to ozone at concentrations which kill leaves (Urbach, pers. comm.).
The simple explanation is that ozone reacts with constitutents of the medium
before it can damage the chloroplasts, even though these are highly sensitive
to oxidants.
Nevertheless, even low concentrations of ozone in air have been observed
to decrease the productivity of birch trees (Matyssek et al. 1992). Apparently,
effects of ozone on photosynthesis are of indirect nature. If forest trees,
where leaves or needles are exposed' to air polluted with ozone during
their life span, do not possess antioxidative defenses which are superior to
those of birch trees (or of spinach), ozone will contribute to forest decline.
Sandermann et al. (1989) summarized subacute effects of ozone on the
metabolism of conifers. He observed that latent damage after fumigation
with ozone found expression only in the following vegetation period
("memory effect").
14.5.4 The Fate of S02
Like N02, S02 may be hydrated already in the aqueous phase of the
apoplasm. Sulfite anions of the resultant sulfurous acid can be oxidized to
sulfite radicals by the oxidized phenolics which are formed in the apoplasm
by the reaction of peroxidase with hydrogen peroxide and apoplasmic
phenolics (Pfanz et al. 1990; Takahama et al. 1993). The radicals are readily
reduced by apoplasmic ascorbate. However, since little or no oxidation of
apoplasmic ascorbate has been observed during fumigation of leaves with
high concentrations of S02 (Takahama et al. 1993), a radical chain oxidation
of sulfite to sulfate seems to be prevented in the apoplasm by ascorbate
(but see Pfanz and Oppmann 1991). Irrespective of what happens in the
apoplasm, the inhibition of photosynthesis observed 1 or 2 min after onset of
fumigation of leaves with high concentrations of S02 (2 to 6ppm, VeljovicJovanovic et al. 1993) shows that S02 and its hydration products rapidly
enter the cytoplasm. Sulfurous acid decreases the cytoplasmic pH, stimulating
the cytoplasmic pH-stat mechanisms which counter acidification (Pfanz et al.
1987; Pfanz and Heber 1989; Pfanz and Heber et al. 1989b; Yin 1990;
Veljovic-Jovanovic et al. 1993). The phosphate translocator of the chloroplast envelope catalyzes not only exchange of phosphate and phosphate
esters between cytosol and chloroplast stroma, but also permits transfer of
sulfite and sulfate (Hampp and Ziegler 1977; Hampp et al. 1980). In the
chloroplasts, sulfite is detoxified either by reduction to the sulfide level or by
oxidation to sulfate (Dittrich et al. 1992). Effective reduction which leads to
the amino acid cysteine depends on the presence of O-acetylserine. Chloroplastic radical scavengers prevent the fast radical chain oxidation of sulfite to