Insect Control: Biological and Synthetic Agents - Index of

136 4: Insect Growth- and Development-Disrupting Insecticides
Figure 13 Schematic representation of titers 20E (thin line) and release of eclosion hormone (EH; dotted line), which triggers the
ecdysis of the larva to complete a normal molt. The solid bold line represents relative titers of ingested tebufenozide in a susceptible
lepidopteran larva (adapted from Dhadialla, unpublished data). Owing to the metabolic stability and amount of tebufenozide in the
insect hemolymph, eclosion hormone, the release of which is normally dependent upon the complete decline of 20E, is not released
and the intoxicated insect is not able to complete the molt, which leads to premature death. Both methoxyfenozide and halofenozide
undergo similar metabolic fate, which is detrimental to intoxicated insect stage. The ecdysone agonists trigger a molt attempt
anytime during the feeding stage of a susceptible larval instar. Events that take place during the molt and are dependent upon the
increasing and decreasing titers of 20E are also shown. The numbers in bold and regular font represent different events triggered
by tebufenozide and 20E, respectively. 1, 1: Inhibition of feeding; 2, 2: initiation of new cuticle synthesis; 3, 3: apolysis of old cuticle
from new cuticle resulting in an ecdysial space filled with molting fluid; 4, 4: head capsule slippage; MI: molt initiated; MC: molt
completed; 5: derailment of the molting process; 6: eclosion hormone is not released, and the larva stays trapped in its old cuticle
and slipped head capsule covering the mouth parts (refer to Figure 9) causing it to starve; 7: molt attempt is lethal and the ecdysone
agonist intoxicated larvae dies of starvation, hemorrhage, and desiccation; 8: cuticle formation continues and molting fluid starts to
be resorbed; 9: molt attempt is completed after release of EH and larva ecdyses into the next larval stage; 10: new cuticle hardens
and the mouth parts are sclerotized so that the larva may continue its growth and development into the next stage.
chromosomal puffs (74EF and 75B), and regression
of pre-existing puffs (25AC, 68C) in larval salivary
glands. In the chromosomal puff assay, the ED50 for
bisacylhydrazine compounds were, however, an
order of magnitude less than for 20E. Results of
additional experiments in this study using different
assays, i.e., glycoprotein glue secretion, imaginal
disc evagination, and rescue of phenotypic expression
in ecdysone deficient mutants showed the
potencies of the bisacylhydrazines were two orders
of magnitude lower than for 20E. In spite of the
quantitative differences in the assays used, the
results confirmed the ecdysone-mimetic action of
the two bisacylhydrazines.
In a study to understand the role of ecdysteroids in
the induction and maintenance of the pharate first
instar diapause larvae of the gypsy moth, Lymantria
dispar, Lee and Denlinger (1997) demonstrated
that a diapause specific 55 kDa gut protein could
be induced in ligature isolated larval abdomens
with injections of either 20E or RH-5992. They
also demonstrated that the effect of KK-42, an imidazole
derivative known to inhibit ecdysteroid biosynthesis,
to prevent prediapausing pharate first
instar larvae from entering diapause could be reversed
by application of 20E or RH-5992. In this
case, RH-5992 was two orders of magnitude more
active than 20E.
Using 1,5-disubstituted imidazoles, Sonoda et al.
(1995) demonstrated that the inductive effects of
these compounds on precocious metamorphosis
of Bombyx mori larvae could be reversed by
tebufenozide.
4.2.4. Basis for Selective Toxicity of
Bisacylhydrazine Insecticides
Unlike halofenozide, which is toxic to both coleopteran
and lepidopteran larvae, both tebufenozide
and methoxyfenozide are selectively toxic to lepidopteran
larvae with a few exceptions of toxicity to