color or become brown or brownish red. By contrast, a chronic injury may be
caused by uptake of sublethal amounts of toxicants over a long period.
Chronic injury is manifested by yellowing of leaves that may progress slowly
through stages of bleaching until most of the chlorophyll and carotenoids are
destroyed.
To cause leaf injury, an air pollutant needs to pass through the stomata of
the epidermal tissue, as the epidermis (Figure 4.2) is the first target for the
pollutant. In passing into the intercellular spaces, the pollutant may dissolve in
the surface water of the leaf cells, affecting cellular pH. A pollutant may not
remain in its original form as it passes into solution. Rather, it may be
converted into a form that is more reactive and toxic than the original
substance. The formation of reactive free radicals following the initial reaction
in the cell is an example. The pollutant, either in its original form or in an
altered form, may then react with specific cellular constituents, such as
cytoplasmic membrane or membranes of the organelles, or with various
substances, including enzymes, coenzymes or cofactors, and substrates. The
pollutant may then adversely affect cellular metabolism, resulting in plant
injury.
3
An example of a gaseous air pollutant widely known for its damaging
effects on plants is SO 2 . Once absorbed into the leaf, SO 2 can induce injuries to
the ultrastructure of various organelles, including chloroplasts and mitochondria, which in turn can lead to disruption of photosynthesis or cellular energy
metabolism. Similarly, histochemical studies of fluoride-induced injury have
indicated that the damage to leaves first occurs in the spongy mesophyll and
lower epidermis, followed by distortion or disruption of chloroplast in the
palisade cells.
4
As a pollutant moves from the substomatal regions to the cellular sites of
perturbation, it may encounter various obstacles along the pathway.
Scavenging reactions between endogenous substances and the pollutant may
occur, and the result may affect pollutant toxicity. For example, ascorbate,
which occurs widely in plant cells, may react with or neutralize a particular
pollutant or a secondary substance formed as the pollutant is metabolized.
Conversely, an oxidant such as O 3 may react with membrane material and
induce peroxidation of the lipid components. This is followed by the formation
of various forms of toxic substances, such as aldehydes, ketones, and free
radicals.
5,6 The free radicals, in turn, may attack cellular components, such as
proteins, lipids, and nucleic acids, which can lead to tissue damage.
Endogenous antioxidants, such as ascorbic acid mentioned above, may react
with free radicals and alter their toxicity.
Cellular enzyme inhibition is often observed when leaves are exposed to
atmospheric pollutants. The inhibition occurs even before the leaf injuries
become apparent. For instance, fluoride (F), widely known as a metabolic
inhibitor, can inhibit a large number of enzymes. Fluoride-dependent enzyme
inhibition is often attributable to reaction of F
À with certain metallic cofactors
such as Cu
2þ or Mg
2þ in an enzyme system. Heavy metals, such as Pb and Cd,
may also inhibit enzymes that contain a sulfhydryl (ÀSH) group at the active
48
Environmental Toxicology
[16:54 26/8/04 P:/CRC PRESS/4365 MING-HO.751 (1670)/4365-004.3d]
Ref: 4365 MING-HO YU Chap-004 Page: 48 45-64
caused by uptake of sublethal amounts of toxicants over a long period.
Chronic injury is manifested by yellowing of leaves that may progress slowly
through stages of bleaching until most of the chlorophyll and carotenoids are
destroyed.
To cause leaf injury, an air pollutant needs to pass through the stomata of
the epidermal tissue, as the epidermis (Figure 4.2) is the first target for the
pollutant. In passing into the intercellular spaces, the pollutant may dissolve in
the surface water of the leaf cells, affecting cellular pH. A pollutant may not
remain in its original form as it passes into solution. Rather, it may be
converted into a form that is more reactive and toxic than the original
substance. The formation of reactive free radicals following the initial reaction
in the cell is an example. The pollutant, either in its original form or in an
altered form, may then react with specific cellular constituents, such as
cytoplasmic membrane or membranes of the organelles, or with various
substances, including enzymes, coenzymes or cofactors, and substrates. The
pollutant may then adversely affect cellular metabolism, resulting in plant
injury.
3
An example of a gaseous air pollutant widely known for its damaging
effects on plants is SO 2 . Once absorbed into the leaf, SO 2 can induce injuries to
the ultrastructure of various organelles, including chloroplasts and mitochondria, which in turn can lead to disruption of photosynthesis or cellular energy
metabolism. Similarly, histochemical studies of fluoride-induced injury have
indicated that the damage to leaves first occurs in the spongy mesophyll and
lower epidermis, followed by distortion or disruption of chloroplast in the
palisade cells.
4
As a pollutant moves from the substomatal regions to the cellular sites of
perturbation, it may encounter various obstacles along the pathway.
Scavenging reactions between endogenous substances and the pollutant may
occur, and the result may affect pollutant toxicity. For example, ascorbate,
which occurs widely in plant cells, may react with or neutralize a particular
pollutant or a secondary substance formed as the pollutant is metabolized.
Conversely, an oxidant such as O 3 may react with membrane material and
induce peroxidation of the lipid components. This is followed by the formation
of various forms of toxic substances, such as aldehydes, ketones, and free
radicals.
5,6 The free radicals, in turn, may attack cellular components, such as
proteins, lipids, and nucleic acids, which can lead to tissue damage.
Endogenous antioxidants, such as ascorbic acid mentioned above, may react
with free radicals and alter their toxicity.
Cellular enzyme inhibition is often observed when leaves are exposed to
atmospheric pollutants. The inhibition occurs even before the leaf injuries
become apparent. For instance, fluoride (F), widely known as a metabolic
inhibitor, can inhibit a large number of enzymes. Fluoride-dependent enzyme
inhibition is often attributable to reaction of F
À with certain metallic cofactors
such as Cu
2þ or Mg
2þ in an enzyme system. Heavy metals, such as Pb and Cd,
may also inhibit enzymes that contain a sulfhydryl (ÀSH) group at the active
48
Environmental Toxicology
[16:54 26/8/04 P:/CRC PRESS/4365 MING-HO.751 (1670)/4365-004.3d]
Ref: 4365 MING-HO YU Chap-004 Page: 48 45-64