Studies on the mechanism of potentiation of the acute toxicity of 2,4-D n-butyl ester and 2′,5-dichloro-4′-nitrosalicylanilide in rainbow trout by carbaryl

Abstract

The acute toxicity of several xenobiotic substances to rainbow trout including 2,4-D n-butyl ester (2,4-DB) and 2′,5-dichloro-4′-nitrosalicylanilide (Bayer 73) has been shown to be potentiated by carbaryl. The effect seen with carbaryl was also observed when arecoline, a direct acting cholinergic agent was substituted for carbaryl. The potentiating effect of both carbaryl and arecoline was abolished by atropine. Carbaryl, at a concentration which potentiates 2,4-DB and Bayer 73, was found to increase the blood and total body concentrations of these compounds during exposures in water. Since carbaryl did not decrease the rate of elimination of 2,4-DB and Bayer 73 from preloaded fish, it appears that carbaryl may increase the acute toxicity of these compounds by increasing their uptake from water by trout. In addition to blocking the increase in acute toxicity seen with carbaryl and arecoline, atropine was also capable of blocking the increase in uptake of 2,4-DB and Bayer 73 produced by carbaryl and arecoline. It was concluded that carbaryl increases the acute toxicity of 2,4-DB and Bayer 73 by increasing the uptake of these compounds from water, possibly by effects on gill blood flow or permeability.