Activity of tralomethrin to modify the nerve membrane sodium channel.
Deltamethrin is a potent type II pyrethroid insecticide which can modify sodium channel gating kinetics in nerve membranes. The actions of another type II pyrethroid tralomethrin to modify sodium channel kinetics have been ascribed to deltamethrin, to which tralomethrin is known to be converted under certain experimental conditions. The objective of this study was to determine if tralomethrin was intrinsically active in modifying the nerve membrane sodium channel, the major target site of pyrethroids. Experiments were performed using the squid giant axon under voltage-clamp conditions. In axons treated with either pyrethroid, a large sodium tail current was generated upon repolarization from a depolarized level and decayed slowly with a dual exponential time course. The fast time constant for tralomethrin was 165 +/- 110 msec and the slow time constant was 3793 +/- 802 msec. For deltamethrin the time constants were significantly shorter, the fast time constant being 34 +/- 6 msec and the slow time constant being 835 +/- 282 msec. The cumulative dose-response relation of tralomethrin revealed two binding sites with apparent dissociation constants of 0.06 and 5 microM. Deltamethrin appeared to bind to only one site with an apparent dissociation constant of 0.25 microM. It is clear that there are large differences in the gating kinetics of the sodium channels modified by tralomethrin and deltamethrin which are incompatible with the idea that tralomethrin is active only after conversion to deltamethrin. The differences in sodium channel gating kinetics after modification by tralomethrin versus deltamethrin indicate that tralomethrin is intrinsically active in modifying the nerve membrane sodium channels.[1]References
- Activity of tralomethrin to modify the nerve membrane sodium channel. Brown, L.D., Narahashi, T. Toxicol. Appl. Pharmacol. (1987) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
