The document outlines various biochemical and physiological target sites of insecticides in insects, detailing how insecticides interact with the nervous system and other physiological functions. It categorizes insecticides based on their mode of action, including neurotoxins and growth regulators, and describes specific chemical classes and their effects on insects. Additionally, it highlights the importance of careful handling and application of insecticides to minimize risks to non-target organisms.

1. BIOCHEMICAL
AND
PHYSIOLOGICAL
TARGET SITES OF
INSECTICIDES IN
INSECTS Submitted By:-
Hemlata
Ph.D scholar
Deptt. of Entomology

2. What are
Insects???
• Insects are tracheate arthropods
whose body is divided into three
regions namely head, thorax and
abdomen possessing two pairs
of wings and three pairs of legs
in thoracic region, genital
organs towards posterior end of
the body and with decentralized
nervous system.
• According to Imm’s

3. INSECTS
• Many insects are considered pests by humans.
• One-sixth of all crops grown worldwide are lost due
to herbivorous insects and the plant diseases they
transmit.
• Insects are responsible for damage to growing crops.

4. INSECTICIDES
• Insecticide may be defined as a
substance or mixture of substances
intended to kill, repel or otherwise
prevent the insects.
• Insecticides are the most powerful
tools available for use in pest
management.
• They are highly effective, rapid in
curative action, adoptable to most
situations, flexible in meeting
changing agronomic and ecological
conditions and economical.

5. • Most of the insecticides commonly used by Pest
Management Professionals can be technically classified
as neurotoxins — i.e., their target site within the target
organism is some aspect of the nervous system.
• The commonly used insecticides, such as insect growth
regulators (juvenile hormone analogs and chitin
synthesis inhibitors) and a few miscellaneous active
ingredients (borates, energy inhibitors and dehydrating
dusts), do not target the nervous system.

6. BIOCHEMICAL TARGET SITE
• Insecticides that do not target the nervous system also
can be subdivided by target site and mode of action, and
include:
1. Muscular calcium channel disruptors
2. Insect growth regulators.
3. Inhibitors of energy production and non-specific
cellular disruptors.
4. Insecticides that act via desiccation (exoskeleton).

7. BIOCHEMICAL TARGET SITE OF
INSECTICIDES
Chemical Group MOA Target Site Route of Entry
Diamides Muscle Stimulation Muscular Calcium channel Oral
Juvenile Hormone Analogs Mimic Juvenile
Hormone Action
JH Degradative Enzymes/
Receptor
Contact & oral
Chitin Synthesis
Inhibitors
Block Chitin
Formation
Exoskeleton Oral
Amidinohydrazones Inhibit Energy production Mitochondria within cells Oral
Pyrroles Inhibit Energy production Mitochondria within cells Contact
Fumigant (sulfuryl
fluoride)
Inhibit Energy
Production
Citric Acid / Glycolysis
Cycles in Cells
Inhalation
Borates Non‐Specific
Metabolic Disruption
Cells Oral
Dehydrating dust Adsorption of
Cuticular Wax Layer
Exoskeleton Contact

8. I.Muscular Calcium Channel toxins
•This includes the active ingredient
chlorantraniliprole.
• It is being developed world-wide
by DuPont belonging to a new class of selective
insecticides featuring a novel mode of action.
• It control a range of pests belonging to the
order Lepidoptera and
someother Coleoptera, Diptera and Isoptera species.

9. Mode of action
• They act on muscular calcium
channels that are under direct
control of the nervous system.
• Diamides bind and stimulate
muscular calcium channels,
causing uncontrolled calcium
release and resultant muscle
contractions.
• Early stages insects appear as
rigid or "contractile" paralysis.

10. II.Insect Growth Regulators
• Insect growth regulators (IGRs) used by the pest management
industry include the juvenile hormone analogs and the chitin synthesis
inhibitors.
• IGRs do not act on the nervous system.
• They disrupt critical physiological functions associated with normal
insect growth, development and reproduction (egg production).
• IGR-containing products generally have low mammalian toxicity (i.e.,
large LD50 values).
• IGRs must be handled safely and applied with a great deal of care and
consideration for non-target organisms.

11. • JHAs may bind to juvenile hormone-degrading enzymes, the juvenile
hormone receptor itself or a combination of both factors.
• The high levels of juvenile hormone within the insect body at a time when it
should not naturally be present.
• This consequences on insect survival and reproduction, severely disrupting
the insect's development and/or altering its reproductive physiology.
• Death or sterilization often results from exposure to JHAs. For example, fire
ant queens exposed to JHA-based baits stop producing eggs and/or colonies
experience a shift in caste composition.
Chemical Class: Juvenile Hormone
Analogs

12. Chemical Class: Chitin Synthesis
Inhibitors
• Chitin synthesis inhibitors do not act on the insect's nervous
system.
• They disrupt an important biochemical pathway responsible for the
synthesis of chitin.
• CSIs used by the structural pest management industry include
diflubenzuron for termite control, and hexaflumuron and
noviflumuron for the control of termites.
• Termite baits that contain chitin synthesis inhibiting insecticides
block chitin formation in molting termites exposed to the active
ingredient.

13. Lufenuron
• Lufenuron is a chitin synthesis inhibitor
used for flea control.
• It is delivered orally and absorbed directly
into the animal's bloodstream.
• These fleas are obligate blood feeders
,consumption of lufenuron results in the
production of eggs that fail to hatch ,since
insect eggs contain chitin, flea larvae are
also killed by lufenuron.

14. Figure. If this food source contains the chitin synthesis inhibitor
lufenuron, then larval fleas cannot properly molt and die when
they molt.Adult female fleas that have fed on lufenuron-
impregnated host blood do not produce viable eggs, but are
themselves unaffected.

15. Buprofezin
• It is a chitin synthesis inhibitor which acts
specifically on sucking pests such as plant hoppers
and whiteflies.
• Its mode of action resembles that of benzoylphenyl
ureas, although its structure is not analogous.
• The compound inhibits incorporation of 3H-
glucose and N-acetyl-D-3H-glucosamine into
chitin .
• The characteristic symptoms in the greenhouse
whitefly result of chitin deficiency, the procuticle
of the whitefly nymphs loses its elasticity and the
insect is unable to molt.

16. Mode of action of CSI’s
• The chitin synthesis inhibitors block an
important enzyme, called chitin synthase.
• This enzyme is directly responsible for
the conversion of certain chemicals into
chitin.
• In the absence of this enzyme, chitin
cannot be synthesized.
• The prevention of chitin synthesis is fatal
for the affected insect.

17. III. Inhibitors of Energy Production and
Non-Specific Cellular Disruptors
• This includes the active ingredient hydramethylnon.
Hydramethylnon is a cellular poison.
• It prevents the mitochondria within cells to produce
energy for the cell and the organism to conduct its
normal activities.
Chemical Class: Amidinohydrazone

18. • Insects exposed to hydramethylnon die slowly as energy
is depleted and not restored.
• The affected insects essentially are depleted of the
energy needed to sustain normal body functions,
causing them to die.
• Insects poisoned by hydramethylnon, as well as the
diamide insecticide chlorantraniloprole, display limp
paralysis much as the inhibitory neurotoxins.
Mode of action

19. Chemical Class: Pyrrole
• This includes the active ingredient chlorfenapyr.
• Indoxacarb, clorfenapyr must be converted by enzymes
within the insect to an active form by a process known
as activation.
• Chlorfenapyr is converted to a new molecule that is
insecticidal.
• These metabolite is toxic to mammals which lack the
necessary enzymes to make the conversion from
inactive to active insecticide.

20. • The mode of action of chlorfenapyr's active metabolite is much like
that of hydramethylnon, i.e., it destroys the mitochondria's ability
to supply energy to meet the insect's needs.
Mode of action

21. Chemical Class: Structural Fumigants
• This includes the active ingredient sulfuryl fluoride.
• In the structural pest control industry, sulfuryl
fluoride is used to fumigate residential and
commercial buildings.

22. Mode of action
• Sulfuryl fluoride inhibits energy production in cells
but does not appear to have a specific target site.
• It is a non-specific metabolic inhibitor that causes a
deprivation of cellular energy.
• Fumigants can be hazardous to applicators and non-
target organisms if mishandled or misapplied.
• A small amount of the warning agent chloropicrin
(tear gas) is applied in residential and commercial
buildings prior to the introduction of sulfuryl
fluoride gas.

23. Chemical Class: Borates
• This includes the active ingredients borax, boric acid
and disodium octaborate tetrahydrate.
• Boron-based active ingredients are exclusively oral
toxicants — they neither exhibit contact toxicity nor
act as cuticular desiccants.
• Borates must either be consumed in baits or
groomed off the insect's body after having been
picked up as a dust formulation.

24. • They are general cellular toxins or non-specific
metabolic disruptors (perhaps even mitochondrial
disruptors).
• These is a feeding deterrent to some pests at high
concentrations, boric acid exhibits excellent water
solubility and is slow acting at low concentrations.
• Disodium octaborate tetrahydrate is an active
ingredient in preventive wood treatments targeted at
both wood-destroying insects and fungi.
Mode of action

25. IV. Insecticides that Act Via Desiccation
• This includes the active ingredients silica gels and diatomaceous
earth.
• Silica gels are synthetically produced, while diatomaceous earth
is the fossilized, skeletal remains of minute microorganisms
known as diatoms.
• Diatoms are unearthed, mined, and used for insect control,
among a myriad of other uses.
• Both silica gels and diatomaceous earth adsorb the thin wax
layer on insect exoskeleton.
Chemical Class: Dehydrating Dusts

26. • The wax layer normally prevents insects from losing
water through their exoskeleton and desiccating.
• By adsorbing the wax layer, silica gels and
diatomaceous earth increase the permeability of the
exoskeleton, resulting in insect death by dehydration.
• Silica gels and diatomaceous earth are most effective
against crawling insects in dry environments where free
water is limited.
Mode of action

27. • The target site of the insect nervous system can be
subdivided based on their specific target site within
the nervous system.
• Specific neurological target sites include sodium and
chloride channels and various components of the
acetylcholine system.
PHYSIOLOGICAL TARGET SITE

28. PHYSIOLOGICAL TARGET SITE OF
INSECTICIDE
Chemical Group MOA Target Site Route of Entry
Pyrethrins /
Pyrethroids
Sodium Channel
Modulation
Axon of nerve Contact
Oxadiazines Sodium Channel blockage Axon of nerve Oral
Semicarbazones Sodium Channel blockage Axon of nerve Oral
OPs / Carbamates Acetyl cholinesterase
inhibition
Nerve Synapse Contact
Neonicotinoids Acetylcholine Receptor
stimulation
Nerve Post‐synapse Contact & Oral
Spinosyns Acetylcholine Receptor
stimulation
Nerve Post‐synapse Oral
Phenylpyrazoles GABA Receptor blockage Nerve Post‐synapse Contact & Oral
Avermectins Glutamate Receptor
stimulation
Nerve Post‐synapse Oral

29. I.Neurological Target Site: Sodium
Channels
• This includes the active ingredients pyrethrins, bifenthrin,
permethrin, cyfluthrin, beta-cyfluthrin, deltamethrin,
cypermethrin, and
lambda-cyhalothrin.
Chemical Class: Pyrethrins and Pyrethroids

30. • Both pyrethrins and pyrethroids disrupt normal nerve function in a
region of the nerve cell known as the axon.
• They inhibit the on/off switch of nerve cells, called sodium
channels, by delaying the rate at which they close, or turn off.
• This results in uncontrolled, uninterrupted nerve firing seen as a
convulsing insect (tremors and shaking) that quickly dies.
• Pyrethroids are toxic to many Hymenoptera (ants, bees and wasps).
• They are easily hydrolyzed (broken down in the presence of
moisture) and are, thus, not very persistent.
Mode of action

31. Chemical Class: Oxadiazines
• This includes the active
ingredient indoxacarb.
Mode of action
• When indoxacarb enters the insect, it is broken down into a new molecule with
insecticidal properties. This process, mediated by enzymes within the insect, is
referred to as activation.
• After activation, the newly formed molecule (called a metabolite) targets sodium
channels along the nerve axon
• The active metabolite tightly binds to the sodium channel, and completely blocks
sodium ion flow into nerve cells.
• Those insects poisoned with indoxacarb appear paralyzed and limp, and are
incapable of movement.

32. Chemical Class: Semicarbazones
• The semicarbazones are a very
new insecticide class.
• This includes the active
ingredient metaflumizone.
• Early indications are that metaflumizone acts similar to the
indoxacarb metabolite.
• It blocks sodium channels and prevents sodium ion
movement into nerve cells.
• The result of this blockage is a loss of neurological function
that is similar to that described for indoxacarb.
Mode of action

33. II. Neurological Target Site:
Acetylcholine System
• These are produced by the process of
esterification between phosphoric acid
and alcohol.
• They undergo hydrolysis with the
liberation of alcohol from the esteric
bond.
• OPs are the main components of nerve gas.
• Eg; dichlorvos chlorpyrifos (Dursban), dichlorvos (DDVP),
malathion, diazinon, acephate (Orthene), propetamphos
(Safrotin) and naled (Dibrom for mosquitoes). etc.
Chemical Class: Organophosphates (OPs)

34. • A carbamate is an organic compound
derived from carbamic acid.
• A carbamate group, carbamate ester,
and carbamic acids are functional groups
that are inter-related structurally and often are interconverted chemically.
• The carbamates are synthetic insecticides modeled after a natural plant toxin (called
physostigmine) from the Calabar bean.
• It cause carbamylation of acetylcholine esterase (AChE) at the level of neuronal
synapses. Their binding to AChE is reversible, and the duration of action is about 24
hours.
• Eg; Carbofuran, aldicarb carbaryl (Sevin), bendiocarb (Ficam), and propoxur
(Baygon). etc.
Chemical Class: Carbamates

35. • OPs and carbamates act by inhibiting the acetylcholinesterase (AchE) enzyme in
the nervous system.
• AchE performs a critical job in the nervous system by removing the neurotransmitter
acetylcholine (Ach) from its receptor on the post-synapse nerve.
• AchE prevents overstimulation of the nervous system because it removes Ach.
without AchE, a stimulated nerve cannot return to its resting state.
• OPs and carbamates tie-up (inhibit) AchE, preventing it from removing Ach from its
receptor site.
• The result is overstimulation of the nerve cell, and death of the insect.
Mode of action

37. Chemical Class: Neonicotinoids
• Neonicotinoids are a new class
of insecticides chemically related
to nicotine.
• The name literally means “new nicotine-like insecticides”.
• The neonicotinoids act on certain kinds of receptors in the nerve synapse.
• They are much more toxic to invertebrates, like insects, than they are to
mammals, birds and other higher organisms.
• Neonicotinoids are synthetic materials modeled after the natural, plant-
produced insecticide nicotine.
• Eg: Imidacloprid, dinotefuran, thiamethoxam, clothianidin and acetamiprid.

38. • Neonicotinoids target the insect nervous system by binding to the
acetylcholine (Ach; a neurotransmitter) receptor on the post-synapse
nerve cell.
• Ach binds to this receptor for only milliseconds (1/1,000 of a second)
at a time, resulting in short and controlled nerve stimulation.
• The neonicotinoids bind to the Ach receptor for very long periods,
approximately minutes or greater.
• This in nerve hyper-stimulation.
• Insects exposed to a neonicotinoid insecticide exhibit symptoms of
tremors and hyperactivity, much like pyrethrins, pyrethroids and
fipronil.
Mode of action

39. Chemical Class: Spinosyns
• This includes the active ingredient
spinosad.
• Spinosyns (also known as
"Naturalytes") are chemicals produced by the soil
bacterium Saccharopolyspora spinosa.
• Spinosyns are acquired by fermentation of S. spinosa
cultures, then by purification and modification of the
active chemical components produced by the microbe.

40. • They primarily targeting binding sites
on nicotinic acetylcholine receptors
(nAChRs) of the insect nervous
system.
• Spinosoid binding leads to disruption
of acetylcholine neurotransmission.
• Spinosad also has secondary effects
as a γ-amino-butyric acid (GABA).
• It kills insects by hyperexcitation.
.
Mode of action
• Spinosyn A
• Spinosyn A initially caused
involuntary muscle contractions
and tremors by widespread
excitation of neurons in the
central nervous system.
• Spinosyn A had no direct
neuromuscular depressant effect
and at very high concentrations
actually enhanced neuromuscular
transmission.
• Spinosyn D
• Spinosoid is a minor component
of spinosad, It acts as an agonist
of insect nicotinic
acetylcholinesterase receptors.

41. III. Neurological Target Site: Chloride
Channels
• Phenylpyrazole insecticides are a class of
chemically-related broad-spectrum insecticides.
Chemical Class: Phenylpyrazole

42. • Fipronil acts on the insect nervous system by binding to and
blocking the GABA receptor on the post-synapse nerve cell.
• This blockage prevents GABA from binding to the receptor
site, which then prevents the influx of chloride ions into the
post-synapse nerve cell.
• These chloride ions limit and balance the electrical activity
within nerve cells, blocking chloride influx leads to rapid,
uncontrolled nerve firing throughout the nervous system.
• Fipronil-treated insects exhibit tremors and shaking.
Mode of action

43. Chemical Class: Avermectins
• This includes the active ingredients
abamectin, emamectin benzoate
and ivermectin.
• The avermectins were originally
isolated from soil bacteria from the genus Streptomyces.
• Older avermectins, such as abamectin, are used in their natural
form; however, newer materials, such as emamectin benzoate,
are partially natural and synthetic. Ivermectin is another
natural avermectin.
• It has uses for endoparasite control in pets and companion
animals.

45. • They bind the chloride channels that are regulated by the
neurotransmitter glutamate.
• While phenylpyrazoles block chloride channels, the
avermectins stimulate them, resulting in constant and
unimpeded chloride ion flow into nerve cells.
• This results in complete inactivation of nerve cells and a loss
of neurological function.
• Poisoning symptoms in insects are similar to those caused by
indoxacarb and metaflumizone (limp paralysis).
Mode of action