Abstract
Esfenvalerate belongs to the pyrethroid group of insecticides which display significant selective toxicity against insects compared to mammalian species, nevertheless, they may pose health risks, especially in case of accidental exposure. The aim of the present study was to model the effect of acute, relatively high-dose exposure of the esfenvalerate-containing formulation Sumi-Alpha?. Eventual functional alterations in the central nervous system and in the gastrointestinal tract were studied on in vitro tissue preparations at different delays after intragastric administration to rats. Neuronal effects were characterized by field potential recording in cortical and hippocampal brain slices, while gastrointestinal effects were examined by analyzing the motility and excitability of isolated ileum segments. On the brain slices originating from esfenvalerate-treated animals, changes in excitability of both inhibitory and excitatory type could be observed. Voltage thresholds necessary to evoke responses in neocortex slices were elevated, and population spike amplitudes were lower in hippocampal slices. However, epileptiform potentials with pronounced late components were also observed. A decreased long-term potentiation (LTP) could be seen in both brain areas after esfenvalerate treatment. Seizure susceptibility of the slices was not significantly altered, but tended to be somewhat higher in slices originating from treated rats. In ileum segments, both spontaneous and acetyl-choline (ACh)-elicited contractions were modified by treatment. Esfenvalerate raised the amplitude of contractions in the low ACh concentration range. However, the solvent xylene also considerably contributed to the detected changes. We can conclude that a relatively high, single oral dose of Sumi-Alpha? exerted mild and temporary effects on the elementary brain functions and intestine functions of the rat.
Highlights
Pyrethroids are widely used insecticides in agriculture, veterinary medicine and public health
Voltage-clamp studies have shown that pyrethroids slow down both activation and inactivation kinetics of the channels, leading to depolarizing after potentials [5]
The aim of the present study was to test the effects of the pyrethroid insecticide esfenvalerate on a mammalian model, the rat
Summary
Pyrethroids are widely used insecticides in agriculture, veterinary medicine and public health. Esfenvalerate was registered in 1986; it contains the most insecticidally active (S,S-) stereoisomer of fenvalerate in high percentage Pyrethroid insecticides exert their effects mainly on the central nervous system, causing hyperactive poisoning symptoms. Their mechanism of action is the modification of the gating kinetics of voltage-gated sodium channels [2]. Voltage-gated sodium channels are responsible for action potential generation in most neurons and other electrically excitable cells, contributing to signal transmission [3] [4]. These channels remain open only for about 1 ms, before being inactivated, closed. If a sufficient fraction of channels is modified, the after potential reaches the cell’s threshold for excitation and repetitive after discharges are produced which are in the background of the poisoning symptoms [6]
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