Jump to main content
Jump to site search

All chapters
Previous chapter Next chapter

Chapter 5

Comparative Metabolism and Toxicology of Pyrethroids in Mammals

Pyrethroid insecticides are toxic to insects and mammals through effects on ion channels in the nervous system, with probable additional sites in muscle. Voltage-gated sodium channels (VGSCs) have been studied most extensively as target sites and there is evidence for two toxicity syndromes (types I and II), associated with different effects on VGSCs, based on the absence or presence of a cyano group in the alcohol moiety. Pyrethroids also have agonist effects on voltage-gated calcium channel subtype(s), which tend to show type I/II differences. There is also evidence for antagonist effects of type II pyrethroids on voltage and GABA-gated chloride channels. Correlations have been made between some ion channel effects and motor activity reductions and effects on the acoustic startle response in the rat. The former is non-specific for type I and II structures but the latter provides some evidence of separation of type I and II. Metabolic transformation of pyrethroids in mammals explains some of the relatively low toxicity of these insecticides in mammals versus insects. Pyrethroids are neurotoxic as the parent; oxidative and hydrolytic metabolites are considered to have little or no toxicity. A wide range of metabolic stability for commercial pyrethroids has been shown. The clinical signs of neurotoxicity following oral gavage dosing in rodents generally correlate with peak blood/plasma concentrations. Similarly, reversibility of neurotoxicity after oral gavage dosing usually occurs within 24h and correlates with large decreases in blood/plasma concentrations.

Publication details


Print publication date
30 Jan 2012
Copyright year
2012
Print ISBN
978-1-84973-191-1
PDF eISBN
978-1-84973-300-7
From the book series:
Issues in Toxicology