Pesticide Metabolism in Plants
43
in plants are simple and complex glucosides, glutathione conjugates and related
products, and amino acid conjugates. In mammals the sulfate, glucuronic acid,
and glutathione-related conjugates often predominate.
2.3.4. 1. Glucose Conjugation
Conjugation of pesticides with glucose in plants usually involves oxidized,
hydrolyzed, or reduced forms of the pesticide in which a free hydroxyl, carboxyl,
or amino group has been exposed so that the conjugation reaction can occur.
Many secondary metabolites of pesticides contain these functional groups that
can be conjugated readily with glucose. Indeed, glucose conjugation is so prevalent with phenolic metabolites of pesticides that the free phenols are rarely
observed in significant concentrations relative to the conjugate forms. The pesticides or their metabolites are normally conjugated as ~-glucosides in plants and
insects. The formation of 0-, N-, and S-glucosides of pesticides has been demonstrated in plants (Baldwin, 1977; Frear, 1975). However, only a few of these
conjugates have been identified unequivocally as glucosides (Frear, 1975). The
primary mechanism for glucosylation appears to involve a UOPG-dependent
glucosyl transferase reaction.
In bean plants, oxidation of the carbamate insecticides, carbaryl (Fig. 2.3),
Baygon® (propoxur), and Banol® (carbanolate) was followed by glucosylation
of the phenol and alcohol metabolites (Kuhr and Casida, 1967). Oxidation and
hydrolysis of the organophosphate BAY NTN 9306® in cotton resulted in the
formation of several phenolic derivatives (Fig. 2.4) that were rapidly conjugated
to apparent glucosides (Bull et ai., 1976). Examples of O-glucosylated herbicides
include chlorprophamm (Still and Mansager, 1972), cisanilide (Frear and Swanson, 1975), and perfluidone (Lamoureux and Stafford, 1977) (Fig. 2.17).
O-glucosylation of oxidized phenolic metabolites of pesticides appears to
be an effective detoxication mechanism. Hydroxylated metabolites of carbamate
insecticides with anticholinesterase activity were inactivated by glucosylation
(Kuhr and Cadisa, 1967). The aryl hydroxylated metabolites of chlorpropham
were reported to be equally active to, or more active than, the parent herbicide
in the inhibition of respiration and phosphorylation activities in isolated plant
mitochondria and the inhibition of firefly luciferase activity (Still et ai., 1974).
The O-glucosides of the hydroxylated metabolites had no inhibitory activity.
Generally, very little of the free phenol forms of pesticides are found in both
susceptible and resistant plants (Frear and Swanson, 1975; Lamoureux and Stafford, 1977; Shimabukuro et ai., 1979; Still et ai., 1974).
Examples of pesticide N- and S-glucosylation in plants are limited (Frear,
1975). The substituted aniline herbicide, chloramben (Amiben®), and other arylamines were glucosylated by a UOP-glucosyl transferase from soybeans that
were specific for the glycosyl donors UOPG and TOPG (Fig. 2.18) (Frear, 1968).
43
in plants are simple and complex glucosides, glutathione conjugates and related
products, and amino acid conjugates. In mammals the sulfate, glucuronic acid,
and glutathione-related conjugates often predominate.
2.3.4. 1. Glucose Conjugation
Conjugation of pesticides with glucose in plants usually involves oxidized,
hydrolyzed, or reduced forms of the pesticide in which a free hydroxyl, carboxyl,
or amino group has been exposed so that the conjugation reaction can occur.
Many secondary metabolites of pesticides contain these functional groups that
can be conjugated readily with glucose. Indeed, glucose conjugation is so prevalent with phenolic metabolites of pesticides that the free phenols are rarely
observed in significant concentrations relative to the conjugate forms. The pesticides or their metabolites are normally conjugated as ~-glucosides in plants and
insects. The formation of 0-, N-, and S-glucosides of pesticides has been demonstrated in plants (Baldwin, 1977; Frear, 1975). However, only a few of these
conjugates have been identified unequivocally as glucosides (Frear, 1975). The
primary mechanism for glucosylation appears to involve a UOPG-dependent
glucosyl transferase reaction.
In bean plants, oxidation of the carbamate insecticides, carbaryl (Fig. 2.3),
Baygon® (propoxur), and Banol® (carbanolate) was followed by glucosylation
of the phenol and alcohol metabolites (Kuhr and Casida, 1967). Oxidation and
hydrolysis of the organophosphate BAY NTN 9306® in cotton resulted in the
formation of several phenolic derivatives (Fig. 2.4) that were rapidly conjugated
to apparent glucosides (Bull et ai., 1976). Examples of O-glucosylated herbicides
include chlorprophamm (Still and Mansager, 1972), cisanilide (Frear and Swanson, 1975), and perfluidone (Lamoureux and Stafford, 1977) (Fig. 2.17).
O-glucosylation of oxidized phenolic metabolites of pesticides appears to
be an effective detoxication mechanism. Hydroxylated metabolites of carbamate
insecticides with anticholinesterase activity were inactivated by glucosylation
(Kuhr and Cadisa, 1967). The aryl hydroxylated metabolites of chlorpropham
were reported to be equally active to, or more active than, the parent herbicide
in the inhibition of respiration and phosphorylation activities in isolated plant
mitochondria and the inhibition of firefly luciferase activity (Still et ai., 1974).
The O-glucosides of the hydroxylated metabolites had no inhibitory activity.
Generally, very little of the free phenol forms of pesticides are found in both
susceptible and resistant plants (Frear and Swanson, 1975; Lamoureux and Stafford, 1977; Shimabukuro et ai., 1979; Still et ai., 1974).
Examples of pesticide N- and S-glucosylation in plants are limited (Frear,
1975). The substituted aniline herbicide, chloramben (Amiben®), and other arylamines were glucosylated by a UOP-glucosyl transferase from soybeans that
were specific for the glycosyl donors UOPG and TOPG (Fig. 2.18) (Frear, 1968).