Insect Control: Biological and Synthetic Agents - Index of

90 3: Neonicotinoid Insecticides
Figure 24 Proposed pathway of acetamiprid metabolism in plants. (Reproduced with permission from Roberts, T.R., Hutson, D.H.
(Eds.), 1999. Metabolic Pathways of Agrochemicals, Part 2, Insecticides and Fungicides. Cambridge University Press, Cambridge.)
The metabolic fate of [2,6- 14 C-pyridine]acetamiprid
was investigated in eggplants and apples following
application to foliage or fruit, and in cabbage plants
after application to foliar and soil. Parent acetamiprid
was slowly metabolized to similar products in
all plants. Acetamiprid was absorbed by and penetrated
the foliage well but it was poorly translocated
(Roberts and Hutson, 1999).
3.7.1.6. Clothianidin Studies of the metabolic
pathway of clothianidin in maize and sugar beet
show a clear and consistent picture (Klein, 2003).
The parent compound is always the major component
of the residue in the edible parts of the
crops. Up to seven metabolites were identified, but
most of them did not exceed 10% of the total radioactive
residues. Furthermore, all the main metabolites
identified in plants were also detected in
rat metabolism studies (Klein, 2003; Yokota et al.,
2003). Generally, the following reactions are
involved in the metabolic pathway of clothianidin
in maize and sugar beets after seed treatment
application:
. N-demethylation to form the N-demethyl clothianidin
and subsequent hydrolysis to produce the
N-(2-chloro-1,3-thiazol-5-ylmethyl)urea;
. hydrolysis of the N0-nitroimino moiety to form
N-(2-chloro-1,3-thiazol-5-yl)-N0-methylurea and
subsequent N-demethylation to form N-(2-chloro-
1,3-thiazol-5-yl)urea;
. denitrification (reduction) to form N-(2-chloro-
1,3-thiazol-5-yl)-N-methylguanidine and C N
w
bond cleavage within the compound to form
N-methylguanidine;
. C w N bond cleavage (loss of the 1,3-thiazol-
5-ylmethyl moiety) to form N-methyl-N 0 -nitroguanidine;
. N-demethylation of N-methyl-N 0 -nitroguanidine
to form N 0 -nitroguanidine;
. denitrification (reduction of N-methyl-N 0 -nitroguanidine
to form N-methylguanidine);
. C w N bond cleavage of N-(2-chloro-1,3-thiazol-
5-yl)-N 0 -nitroguanidine to form nitroguanidine;
and
. C w N bond cleavage (loss of the N 0 -nitroimino
moiety) and subsequent oxidation of the
intermediate to form 2-chloro-1,3-thiazol-5carboxylic
acid.
Unchanged parent compound is the major constituent
of the residue at harvest. The major pathway
of metabolism involves N-demethylation of
clothianidin to produce N-(2-chloro-1,3-thiazol-
5-ylmethyl)-N 0 -nitroguanidine. In some crop parts
N-methylguanidine made up some 20% of the
residue at harvest (Klein, 2003).
3.8. Pharmacology and Toxicology
Because of the target site selectivity, neonicotinoids
are more toxic to aphids, leafhoppers, and other
sensitive insects than to mammals and aquatic life
(Matsuda et al., 1998; Yamamoto et al., 1998;
Tomizawa et al., 2000; Tomizawa and Casida,
2003). Comparative binding studies on insects
nAChRs indicate that their ability to displace tritiated
imidacloprid from its binding site correlates
well with their insecticidal efficacy (Kagabu,
1997a; Nauen et al., 2001).