endrin and fenvalerate

Fathead minnow larvae (Pimephales promelas) were exposed to three individual pesticides during brief or continuous exposure in 96-hr and 28- to 30-day toxicity tests. Continuous exposure 96-hr LC50 values for chlorpyrifos, endrin, and fenvalerate were 122.2, 0.7, and 0.85 micrograms/liter, respectively. Continuous exposure chronic effect concentrations were chlorpyrifos, 2.1 micrograms/liter (increased deformities); endrin, 0.38 micrograms/liter (reduction in growth); and fenvalerate, 0.36 micrograms/liter (reduction in survival and growth). Brief exposure chronic test results indicated that fathead minnow exposure to chlorpyrifos for as few as 5 hr at a concentration similar to a continuous exposure 96-hr LC50 value resulted in increased deformities and a reduction in growth, whereas a 48-hr exposure at a concentration similar to a continuous exposure 96-hr LC50 value was required to cause a reduction in growth for endrin and a reduction in survival and growth for fenvalerate. It is suggested that although constant exposure laboratory tests are essential for hazard assessment, the relationships of exposure duration and toxicant intensity to ecotoxic effects are necessary for reliable risk assessments and implementation of water quality standards.

Topics: Animals; Chlorpyrifos; Cyprinidae; Endrin; Lethal Dose 50; Nitriles; Pyrethrins; Water Pollutants; Water Pollutants, Chemical

The effects of various classes of insecticides were studied on the N-demethylation of dimethylnitrosamine (DMN) by mouse liver enzymes. Organochlorine insecticides, represented by lindane, DDT, and endrin, increased the activities of DMN demethylase I and II. The latter enzyme was more susceptible to the inducive action of the tested chlorinated insecticides. On the other hand, the synthetic pyrethroids, fenvalerate and flucythrinate, did not alter the activity of either enzyme. While pretreatment with carbaryl, a carbamate derivative, was without effect, moderate elevation in the activity of both demethylases was observed following administration of carbofuran. Dimethoate, representing organophosphorus compounds, was the only insecticide tested to inhibit the N-demethylation of DMN, with more pronounced effect on DMN demethylase I. Since DMN requires metabolic activation for its hepatotoxic and carcinogenic actions, alterations in the activities of its metabolizing enzymes as a sequela of exposure to certain insecticides may change susceptibility to its toxicity and/or carcinogenicity.

Topics: Animals; Carbaryl; Carbofuran; Cytochrome P-450 CYP2E1; DDT; Dimethoate; Dimethylnitrosamine; Endrin; Hexachlorocyclohexane; Insecticides; Liver; Male; Mice; Nitriles; Oxidoreductases, N-Demethylating; Pyrethrins