Paresthesia From Cutaneous Exposure to a Synthetic Pyrethroid Insecticide

Knox, J. Marshall

doi:10.1001/archderm.1984.01650420054015

Cited by 36 publications

(11 citation statements)

References 8 publications

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“…The other earlobe was treated with the vehicle only and served as a control. 163 In a subsequent study four formulation grade pyrethroid insecticides were diluted in distilled water and applied to the earlobe (130 pg/cm2) of six human volunteers. Permethrin caused the least and flucythnnate the most pronounced paresthesia, whereas the two intermediate compounds fenvalerate and cypermethrin gave almost equal cutaneous sensations.…”

Section: Human Studiesmentioning

confidence: 99%

Neurotoxicological Effects and the Mode of Action of Pyrethroid Insecticides

Vijverberg¹,

Bercken²

1990

Critical Reviews in Toxicology

347

137

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Neuroexcitatory symptoms of acute poisoning of vertebrates by pyrethroids are related to the ability of these insecticides to modify electrical activity in various parts of the nervous system.Repetitive nerve activity, particularly in the sensory nervous system, membrane depolarization, and enhanced neurotransmitter release, eventually followed by block of excitation, result from a prolongation of the sodium current during membrane excitation. This effect is caused by a stereoselective and structure-related interaction with voltage-dependent sodium channels, the primary target site of the pyrethroids.Near-lethal doses of pyrethroids cause sparse axonal damage that is reversed in surviving animals. After prolonged exposure to lower doses of pyrethroids axonal damage is not observed.Occupational exposure to pyrethroids frequently leads to paresthesia and respiratory irritation, which are probably due to repetitive firing of sensory nerve endings. Massive exposure may lead to severe human poisoning symptoms, which are generally treated well by symptomatic and supportive measures.

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Section: Human Studiesmentioning

confidence: 99%

Neurotoxicological Effects and the Mode of Action of Pyrethroid Insecticides

Vijverberg¹,

Bercken²

1990

Critical Reviews in Toxicology

347

137

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“…Increased cough rate may have been a function of the morphological changes in the gill or may have been due to interactions of fenvalerate with pharngeal receptors. Fenvalerate has been reported to cause skin paresthesias in humans, seemingly because of effects on sensory nerves (Cagen et al 1984;Knox et al 1984). Finally, urine osmolality and urinary Na+ and K+ excretion rates and concentrations were significantly elevated in intoxicated trout, which suggests that fen valerate may also interfere with renal ion regulation.…”

Section: B Signs Of Intoxication and Physiological Responsesmentioning

confidence: 99%

Comparative Toxicology of the Pyrethroid Insecticides

Bradbury¹,

Coats

1989

Reviews of Environmental Contamination and Toxicology

278

142

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“…The NMDA receptor, which is an ionotropic receptor that is modulated by voltage-dependent Mg 2+ blockage and possesses a Ca 2+ channel, is one of the excitatory glutamate receptors [7]. Additionally, the NMDA receptor is likely related to the long-term potentiating action of dopamine [4,7].Male Sprague-Dawley (SD) rats weighing 220-290 g (7-10 weeks of age) obtained from Japan SLC Laboratory (Hamamatsu, Japan) were used in this investigation. The animals were housed in plastic cases in a ventilated room with a controlled temperature (23  2C), relative of humidity (55  22%) and 12-hr light/dark cycle of the artificial light.…”

mentioning

confidence: 99%

“…Although pyrethroids were found to show differential effects on the nervous system [6] as mentioned above, a high dose of deltamethrin has been thought to increase extracellular dopamine levels during the late response phase [4]. The NMDA receptor, which is an ionotropic receptor that is modulated by voltage-dependent Mg 2+ blockage and possesses a Ca 2+ channel, is one of the excitatory glutamate receptors [7]. Additionally, the NMDA receptor is likely related to the long-term potentiating action of dopamine [4,7].…”

mentioning

confidence: 99%

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Effects of the NMDA Receptor Antagonists on Deltamethrin-Induced Striatal Dopamine Release in Conscious Unrestrained Rats

Morikawa

Furuhama

2009

The Journal of Veterinary Medical Science

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ABSTRACT. To better understand the neurotoxicity caused by the pyrethroid pesticide, we examined the effects of the N-methyl-D-aspartate (NMDA) receptor antagonists MK-801, a non-competitive cation channel blocker, and 2-amino-5-phosphonovaleric acid (APV), a competitive Na + channel blocker, on extracellular dopamine levels in male Sprague-Dawley rats receiving the type II pyrethroid deltamethrin using an in vivo microdialysis system. Deltamethrin (60 mg/kg, i.p.) evidently increased striatal dopamine levels with a peak time of 120 min, and the local infusion (i.c.) of either MK-801(650 M) or APV (500 M) completely blocked these actions. The fluctuation in the dopamine metabolite 3-MT also resembled that in dopamine. Our results suggest that dopamine-releasing neurons would be modulated via the NMDA receptor by the excitatory glutamatergic neurons after deltamethrin treatment.KEY WORDS: deltamethrin, microdialysis, rat, striatal dopamine.J. Vet. Med. Sci. 71(8): 1129-1132, 2009 Pyrethroids have been chemical-structurally classified into two groups; type I pyrethroids (e.g. allethrin and pyrethrin) lack a cyano moiety, and type II pyrethroids (e.g. deltamethrin and cyhalothrin) possess a cyano group in the -position [6]. However, these classifications have several shortcomings, because common toxic syndromes in mammals are different for the respective types [4,6,11]. Since type II synthetic pyrethroid esters have exhibited a highly selective toxicity without leaving a residue, they have been widely used as a pesticide [6]. As the pharmacological action of the pyrethroids including deltamethrin, it has been shown that they modify the gating kinetics of axonal Na + channels involved in the inward flow of Na + ions, producing the action potential in cells that are normally closed at the resting potential [6,[8][9][10]. Most recently, it has been reported that deltamethrin stimulates the glutamate receptor, or blocks the -aminobutyric acid (GABA A ) receptor [5], presumably leading to chronic seizures [6]. In the present work, to better understand the neurotoxicity induced by the pyrethroid, we used an in vivo microdialysis system to examine the effects of the N-methyl-D-aspartate (NMDA) receptor antagonists MK-801, a non-competitive cation channel blocker, and 2-amino-5-phosphonovaleric acid (APV), a competitive Na + channel blocker, on extracellular dopamine levels in conscious unrestrained male rats receiving the type II pyrethroid pesticide deltamethrin. Although pyrethroids were found to show differential effects on the nervous system [6] as mentioned above, a high dose of deltamethrin has been thought to increase extracellular dopamine levels during the late response phase [4]. The NMDA receptor, which is an ionotropic receptor that is modulated by voltage-dependent Mg 2+ blockage and possesses a Ca 2+ channel, is one of the excitatory glutamate receptors [7]. Additionally, the NMDA receptor is likely related to the long-term potentiating action of dopamine [4,7].Male Sprague-Dawley (SD) rats weighing 220-...

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Paresthesia From Cutaneous Exposure to a Synthetic Pyrethroid Insecticide

Cited by 36 publications

References 8 publications

Neurotoxicological Effects and the Mode of Action of Pyrethroid Insecticides

Neurotoxicological Effects and the Mode of Action of Pyrethroid Insecticides

Comparative Toxicology of the Pyrethroid Insecticides

Effects of the NMDA Receptor Antagonists on Deltamethrin-Induced Striatal Dopamine Release in Conscious Unrestrained Rats

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