1. ROTENONE
Rotenone is an odourless, colourless , crystalline
ketonic chemical compound used as a broad-
spectrum insecticide, piscicide, and pesticide. It occurs
naturally in the seeds and stems of several plants, such as
the jicama vine plant; and the roots of several members
of Fabaceae.

2. hexahydro-2-isopropenyl-8,9-
dimethoxychromeno[3,4-b]
furo(2,3-h)chromen-6-one
Molecular formula C23H22O6
Rotenone is produced
by extraction from the
roots and stems of
several tropical and
subtropical plant
species, especially
those belonging to the
genera Lonchocarpus
and Derris.

3. • The active chemical component was first isolated by a
French botanist Emmanuel Geoffroy in 1895 and called
it nicouline, from a specimen of Robinia nicou, now
called Lonchocarpus nicou, while traveling in French
GuianaIn 1902, a Japanese chemist, Nagai isolated a pure
crystalline compound from Derris elliptica which he called
rotenone, after the Japanese name of the plant roten. By
1930, nicouline and rotenone were established to be
chemically the same.[

4. Mechanism of action
Rotenone works by interfering with the electron
transport chain in mitochondria. To be specific, it
inhibits the transfer of electrons from iron-sulfur
centers in complex I to ubiquinone. This interferes
with NADH during the creation of usable cellular
energy (ATP). Cellular oxygen is reduced to the
radical, creating a Reactive Oxygen Species, which
can damage DNA and other components of the
mitochondria

5. Uses
• Rotenone is used as a pesticide, insecticide, and as a
nonselective piscicide
• It is commercialized as cubé, tuba, or derris, in single
preparation or in synergistic combination with other
insecticides.
• Rotenone has historically been used by indigenous peoples to
catch fish. Typically, rotenone-containing plants in
the Fabaceaefamily of legumes are crushed and introduced
into a body of water, and as rotenone interferes with cellular
respiration, the affected fish rise to the surface in an
attempt to gulp air, where they are more easily caught.

6. • Rotenone is also used in powdered form to
treat scabies and head lice on humans,
and parasitic mites on chickens, livestock, and pet animals.
• Rotenone has been used as an organic pesticide dust for
gardens
• It kills potato beetles, cucumber beetles, flea beetles, cabbage
worms, raspberry beetles, and asparagus beetles, as well as
most other arthropods. It rapidly biodegrades under warm
conditions, so harmful residues are minimal. A light dusting on
the leaves of plants will control insects for several days.

7. Toxicity
• It is mildly toxic to humans and other mammals, but
extremely toxic to insects and aquatic life, including fish.
This higher toxicity in fish and insects is because
the lipophilic rotenone is easily taken up through
the gills or trachea, but not as easily through the skin or
thegastrointestinal tract. Rotenone is toxic to erythrocytes in
vitro. The lowest lethal dose for a child is 143 mg/kg. Human
deaths from rotenone poisoning are rare because its
irritating action causes vomiting Deliberate ingestion of
rotenone can be fatal

8. • The compound decomposes when exposed to
sunlight and usually has an activity of six days in
the environment.It oxidises to rotenolone, which is
less toxic than rotenone. In water, the rate of
decomposition depends upon several factors,
including temperature, pH, water hardness and
sunlight. The half-life in natural waters ranges
from half a day at 24°C to 3.5 days at 0°C.

9. Pyrethroids
+
=
Piperonyl butoxide

10. Pyrethroids
• Derived from pyrethrins;
natural compounds produced
by chrysanthemum flowers (C.
cinerariaefolium and C.
cineum
• Pyrethrins will paralyze insect;
animal will recover (enzyme
detoxification)
• Pyrethroids are synthetic
esters derived from pyrethrins;
engineered for insect death,
“knockdown” effect
• Synthetic modifications
(addition of synergists) make
these compounds more toxic to
organisms, less degradable in
environment

11. Pyrethroid
Structures
• Pyrethrins are esters of
chrysanthemic (I) or
pyrethric (II) acid; have
been synthetically
modified into complex
mixture of isomers
• Type 1 and 2 pyrethroids
• Very lipophillic, low
water solubility
• Structure of compound (I
or II) has different effects
and associated poisoning
symptoms
• Isomerism around the
cyclopropane ring greatly
influences toxicity
All pyrethroids have an acid moiety, a
central ester bond, and an alcohol moiety
Permethrin

12. • Pyrethroids are synthetic
analogs of pyrethrins, made
to last longer and be more
toxic to insects.
• Type I – shorter duration of effects
• Type II – longer acting, enhanced by
addition of cyano group
• Type I - pesticides
Pyrethrins,bioallethrin,cismeth
rin
Type I -
poisonings
•Severe fine tremor
• Marked reflex
hyperexcitability
• Sympathetic
activation
• Paresthesia
(dermal exposure)

13. • Type II (cyano) - pesticides
• fenvalerate
• cyhalothrin
• deltamethrin
• cypermethrin
Type II - poisonings
• Profuse watery salivation
• Coarse tremor
• Sympathetic activation
• Choreoathetosis
• Seizures (dermal exposure)

14. Uses of pyrethroid
• Domestic – e.g. bug bombs, mosquito nets, insect sprays
• Medical - e.g. treatment of scabies and lice
• Commercial – e.g. insecticide for agriculture
• Veterinary – e.g. pet shampoos, fleas

16. Mode of entry into
aquatic environment
• Spray drift; pyrethroids often applied
aerially and can contaminate nearby
waters
• Runoff from fields, wastewater from
manufacturing facilities

17. Mode of Entry into Organisms
• Rapidly absorbed to particulate matter in water due
to high lipophillicity/low solubility
• Half life for pyrethroids in aquatic medium has
been reported between 19 hours
• Most pyrethroid half lives in water range from 1-2
days
• Its speciation varies greatly with compound’s
structure, exposure to sunlight, and pH,
temperature, and salinity of water medium
• Since pyrethroids are highly lipophillic, will readily
be absorbed through the gills of aquatic animals
• In mammals, toxicity occurs when ingested, not
readily absorbed through skin

18. • Absorption:
• GI: moderate
• Respiratory Tract: moderate
• Dermal: poor
• Usually metabolized quickly by the liver
• Excreted primarily in urine, less in feces
• Half life – usually 5-20 hours, can be days
• Often combined with synergist (e.g. piperonyl) to
enhance killing power & slow degradation
• Lipophilic, may concentrate in fat tissues

19. Mechanism of Action
Acts primarily on voltage dependent sodium
channels leading to hyperexcitable state, also
affects chloride channels to increase excitability
• Increases adrenal activation – increasing
adrenaline
• Duration of effect is determined by the structure of
the offending pyrethroid

20. Mode of Toxic Interaction:
Neurotoxicity
• Acute neurotoxicity is caused by binding to sodium channels--> slows
down its activation and inactivation properties which leads to a
hyperexcitable state
• A normal action potential is converted into double or continuous
discharges in nerve and muscle
• Current duration dependant on pyrethroid structure; action
stereospecific
• Insect sodium channels 100x more susceptible than mammals

21. Other Toxic Interactions
• Most pyrethroids stimulate protein kinase C-
dependant protein phosphorylation (channel
activity modulated by phosphorylation state)
• Antagonism of GABA-mediated inhibition (seizures)
• Enhancement of noradrenalin release
• Direct actions on calcium or chloride ion channels
(type II only)
• Type II pyrethroids produce a more complex
poisoning syndrome and act on wider range of
tissues

22. Metabolism and Breakdown
• Biological activity destroyed by ester hydrolysis,
major route, creates oxidative metabolites
• Oxidative reactions catalyzed by cytochrome P450
(CYP) enzymes in all animals (CYP6 family important
for insects). Is thought that insecticidal properties of
pyrethroids terminated by oxidative metabolism .
Resistance to pyrethroids due to detoxification by CYP
monooxygenases
• Resistance associated with elevated CYP activity.