BOB MARTIN TICK AND FLEA SHAMPOO (DOG)

Indications

• Synergist in pesticide formulations
• Enhancement of insecticidal activity

Dosage

Children: Refer to specific pesticide formulations for guidance, as piperonyl butoxide is not used as a standalone medication.

Adults: Refer to specific pesticide formulations for guidance, as piperonyl butoxide is not used as a standalone medication.

Mechanism of action

Piperonyl butoxide acts as a synergist by inhibiting the mixed-function oxidase (MFO) system of insects, which enhances the activity of pesticides and allows for lower doses of insecticides to be used effectively. This mechanism increases the levels of insecticides within the target organism, thereby improving their lethality without increasing the dosage of the insecticide.

Pharmacodynamics

Piperonyl butoxide does not affect the mixed-function oxidase system in humans and has shown no significant effects in small trials involving human volunteers. Its primary action is limited to insects, where it enhances the toxicity of certain insecticides by preventing their breakdown.

Pharmacokinetics

The pharmacokinetics of piperonyl butoxide in humans is not well-studied, and it does not significantly interact with human metabolic pathways like the mixed-function oxidase system. Its effects are predominantly observed in insects where it alters the metabolism of co-administered pesticides.

Pregnancy

Piperonyl butoxide should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. Data on the effects of piperonyl butoxide in pregnant women are limited.

Breast-feeding

There is insufficient data on the excretion of piperonyl butoxide in human milk. Caution should be exercised when administering to breastfeeding women.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Formulations

• Piperonyl butoxide 30% concentration for agricultural use
• Piperonyl butoxide formulations combined with insecticides such as pyrethrins and carbamates

Indications

• Control of agricultural pests
• Public health pest control
• Vector control for diseases transmitted by insects

Dosage

Children: Refer to specific guidelines based on the formulation and target pest, as dosages can vary widely. Consult the product label or BNF for precise dosing information.

Adults: Refer to specific guidelines based on the formulation and target pest, as dosages can vary widely. Consult the product label or BNF for precise dosing information.

Mechanism of action

Cypermethrin exerts its effects primarily at voltage-sensitive sodium channels in both insect and mammalian neurons. It enhances the binding of specific ligands to these channels, leading to prolonged depolarization of the neuron and disruption of normal nerve function. Additionally, cypermethrin may also act on the gamma-aminobutyric acid (GABA) receptor-chloride ionophore complex, further contributing to its neurotoxic effects.

Pharmacodynamics

As a pyrethroid, cypermethrin has a high affinity for sodium channels, which causes sustained activation and subsequent paralysis of the insect’s nervous system. This mechanism results in the inability of the insect to coordinate movement or respond to stimuli, ultimately leading to death. The insecticidal potency is influenced by the stereochemistry of the compound, with different isomers demonstrating varying levels of effectiveness.

Pharmacokinetics

Cypermethrin is absorbed through the exoskeleton of insects and can also be absorbed through the skin in mammals. Once in the system, it is metabolized in the liver, with metabolites excreted primarily in urine. The compound has a relatively low bioavailability in mammals and is rapidly eliminated. Environmental factors such as temperature and moisture can influence its degradation and persistence in the environment.

Adverse effects

• Skin irritation
• Respiratory issues
• Nausea
• Headache
• Dizziness

Precautions

• Use with caution in patients with known hypersensitivity to pyrethroids
• Avoid contact with eyes and mucous membranes
• Use personal protective equipment when handling

Pregnancy

Cypermethrin should be used in pregnancy only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

It is not known whether cypermethrin is excreted in human milk; caution should be exercised when administering to breastfeeding women.

Storage

Store in a cool, dry place, away from direct sunlight and heat. Keep out of reach of children.

Formulations

• Liquid concentrate
• Aerosol spray
• Emulsifiable concentrate

Indications

• Insecticide synergist in agricultural pest control
• Potential therapeutic applications in various medical fields

Dosage

Children: Refer to specific product guidelines as dosing can vary widely based on formulation and intended use.

Adults: Refer to specific product guidelines as dosing can vary widely based on formulation and intended use.

Mechanism of action

Piperony functions by inhibiting cytochrome P450 enzymes in insects, which are responsible for the metabolism of various insecticides. By blocking these enzymes, piperony increases the toxicity of the insecticides that would otherwise be rapidly detoxified, thereby enhancing their efficacy.

Pharmacodynamics

Piperony has a synergistic effect when combined with other insecticides, increasing their potency and prolonging their action. This mechanism allows for effective pest control while minimizing the amount of active insecticide required, which can reduce potential toxicity to non-target organisms.

Pharmacokinetics

Piperony is absorbed through the skin and gastrointestinal tract when ingested. It is metabolized in the liver and primarily excreted through the kidneys. The half-life and distribution in the body can vary based on the formulation and route of exposure, but specific pharmacokinetic data for piperony is limited in the literature.

Pregnancy

There is limited information on the safety of piperony during pregnancy. It is advisable to avoid use unless clearly needed and prescribed by a healthcare professional.

Breast-feeding

There is insufficient data on the excretion of piperony in human milk. Caution is recommended when administering to breastfeeding women.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Mechanism of action

Piperonyl butoxide is not a pesticide, but acts as a synergist to increase the activity of pesticides such as carbamates, pyrethrins, pyrethroids, and rotenone. Piperonyl butoxide inhibits the mixed-function oxidase (MFO) system of an insect. The MFO system is the insects natural defense system and causes the oxidative breakdown of insecticides. Thus, by inhibiting this system piperonyl butoxide promotes higher levels of insecticide and allows for lower doses to be used for a lethal effect. To clarify the mechanism of piperonyl butoxide (PBO)-induced hepatocarcinogenesis in mice, male mice were subjected to a two-thirds partial hepatectomy, N-diethylnitrosamine (DEN) initiation, and a diet containing 0.6% PBO for eight weeks. The incidence of gamma-glutamyl transpeptidase (GGT)-positive foci and PCNA-positive cells was significantly increased in the DEN + PBO group compared with the DEN-alone group. Real-time reverse transcription-polymerase chain reaction (RT-PCR) analysis showed up-regulation of genes related to metabolism, such as cytochrome P450 1A1 and 2B10, and metabolic stress, such as Por, Nqo1, Nrf2, abcc3, and abcc4. Early responsive genes downstream of mitogen-activated protein kinase (MAPK), such as c-fos, c-jun, c-myc, and activating transcription factor 3 (ATF3), were also up-regulated in this group. Positive immunohistochemical staining for ATF3 was diffusely observed in nonproliferating hepatocytes of the DEN + PBO group, but altered foci were negative or weakly positive for ATF3. The nuclei of hepatocytes within ATF3-negative foci were positive for cyclin D. Thus PBO can induce oxidative stress, activate the MAPK pathway, and increase ATF3 transcript levels in hepatocytes outside the altered foci during the early stage of PBO-induced hepatocarcinogenesis in mice. . ... Male F344 rats were administered piperonyl butoxide mixed in the diet at concentrations of 0 (negative control), 0.05, 0.2 or 2% for 2 days, 1, 2, and 4 weeks. As a positive control, phenobarbital was administered to rats for up to 4 weeks as a 0.1% solution in the drinking water. Increased liver weight, centrilobular hepatocellular hypertrophy due to increased smooth endoplasmic reticulum, decreased numbers and areas of connexin 32-positive spots per hepatocyte, and increased cell proliferation were observed in rats treated with 0.2 and 2% piperonyl butoxide. Similar results were obtained for 0.1% phenobarbital treated rats. Hepatocellular necrosis suggestive of hepatotoxicity was also observed in the 2% piperonyl butoxide group. These results indicate that the promoting mechanism of piperonyl butoxide in hepatocarcinogenesis is similar to that of phenobarbital, involving an ability to induce CYP isoenzymes and inhibit gap junctional intercellular communication. In addition, increased cell proliferation following hepatocellular necrosis may also play a role at high doses. Piperonyl butoxide (PBO) is an insecticide synergist known to inhibit the activity of cytochrome P450 enzymes. ... Little is known about how insects respond to PBO exposure at the gene transcription level. The authors have characterized the transcriptional response of the Drosophila melanogaster genome after PBO treatment, using both a custom-designed 'detox' microarray, containing cytochrome P450 (P450), glutathione S-transferase (GST) and esterase genes, and a full genome microarray. A subset of P450 and GST genes is identified, along with additional metabolic genes, that are induced by PBO. The gene set is an extremely similar gene set to that induced by phenobarbital, a compound for which pretreatment is known to confer tolerance to a range of insecticide compounds. Piperonyl butoxide (PBO), alpha-[2-(2-butoxyethoxy)ethoxy]-4,5-methylene-dioxy-2-propyltoluene, is widely used as a synergist for pyrethrins. In order to clarify the possible mechanism of non-genotoxic hepatocarcinogenesis induced by PBO, molecular pathological analyses consisting of low-density microarray anal

Pharmacodynamics

Piperonyl butoxide does not affect the mixed-function oxidase system in humans. In small trials in human volunteers, usual doses of piperonyl butoxide had no effect on humans.

Mechanism of action

Pyrethroid insecticides are synthetic neurotoxins patterned after the naturally occurring pyrethrins. Their mechanism of action is thought to involve effects primarily at the voltage-sensitive sodium channel of both insect & mammalian neurons, although recent studies have raised the possibility that these cmpds may also act at the gamma-aminobutyric acid receptor-chloride ionophore complex. Here we show that active pyrethroids of the alpha-cyano-3-phenoxybenzyl class allosterically enhance the binding of (3)H-batrachotoxinin-A 20-alpha-benzoate to voltage-sensitive sodium channels of rat brain in a dose-dependent & stereospecific manner. Comparison of the rank order of potency for enhancement of (3)H-batrachotoxinin-A 20-alpha-benzoate binding & insecticidal activity in a series of toxic steroisomers of cypermethrin, representative of the class, reveals a correlation between the two measures. These results support a sodium channel site model for pyrethroid action & suggest a useful & practical method to help evaluate the relationship between the sodium channel & insecticidal potency for members of this class of cmpds. Following absorption through the chitinous exoskeleton of arthropods, pyrethrins stimulate the nervous system, apparently by competitively interfering with cationic conductances in the lipid layer of nerve cells, thereby blocking nerve impulse transmissions. Paralysis and death follow. /Pyrethrins/ The efforts of this study were directed at defining the importance of esterases, mixed function oxidases and mitochondrial respiratory chain enzymes in in vitro covalent binding of cismethrin and the two cyanopyrethroids, cypermethrin and deltamethrin to phenobarbital induced rat liver homogenate and microsomes. Each enzyme system was selectively inhibited to elucidate the activation mechanism involved. Piperonyl-butoxide and carbon-monoxide were used to inhibit mixed function oxidases. Tetraethylpyrophosphate inhibited esterase and trichloropropene-oxide inhibited epoxide-hydrolase. Potassium cyanide or rotenone was used to block the mitochondrial electron transport. The study demonstrated that covalent binding of cismethrin, cypermethrin, and deltamethrin was dependent on pyrethroid concentration. Inhibition of esterases and mitochondrial respiration only slightly altered the covalent binding level. Inhibition of cytochrome p450 and mixed function oxidases reduced the covalent binding, making it almost nonexistent. The covalent binding was decreased by 50% through an 80% inhibition of epoxide-hydrolase. In vitro, the comparison of data between alcohol and acid labeling of the same pyrethroid suggested that the whole molecule was bound to proteins in an activation process, perhaps epoxidation, and that hydrolysis could only occur afterwards. The role of cytochrome p450 dependent monooxygenases in the covalent binding process was stressed. Interaction with sodium channels is not the only mechanism of action proposed for the pyrethroids. Their effects on the CNS have led various workers to suggest actions via antagonism of gamma-aminobutyric acid (GABA)-mediated inhibition, modulation of nicotinic cholinergic transmission, enhancement of noradrenaline release, or actions on calcium ions. Since neurotransmitter specific pharmacological agents offer only poor or partial protection against poisoning, it is unlikely that one of these effects represents the primary mechanism of action of the pyrethroids, & most neurotransmitter release is secondary to incr sodium entry. /Pyrethroids/ For more Mechanism of Action (Complete) data for CYPERMETHRIN (12 total), please visit the HSDB record page.