Inhibition of in vivo and in vitro epoxidation of aldrin, and potentiation of toxicity of various insecticide chemicals by diquat in two species of fish.

Abstract

Diquat (1,1′-ethylene-2,2′-dipyridylium dibromide), a potent contact herbicide useful in aquatic weed control, inhibits aldrin epoxidation, an oxidative transformation catalyzed by microsomal mixed—function oxidases. When live mosquito fish (Gambusia affinis) are exposed to sublethal amounts of aldrin in the water for 24 hours, the chlorohydrocarbon residue extracted from the whole fish contains approximately 23 percent of the epoxide, dieldrin. Addition of diquat to the water in final concentration of 8 × 10−4 molar or greater significantly reduces the percent dieldrin in the extracted residue. Underin vitro conditions, diquat inhibits the aldrin epoxidase system prepared from homogenates of various tissues in mosquito fish and goldfish(Carassius auratus); a diquat concentration of 2 × 10−5 molar in enzyme systems prepared from liver, stomach, intestine, kidney, and gill homogenates from goldfish gives 74, 55, 18, 41, and 57 per cent inhibition, respectively. The inhibition is concentration dependent, the molar I50 for liver preparations being 8.0 × 10−6 molar. Under static bioassay conditions, the acute toxicities of aldrin, DDT, and parathion are not affected by diquat but diquat (275 ppm) decreases the time to onset of symptoms and increases the 24—hour mortalities produced by carbaryl, the effects being dose—dependent. In view of the high concentration of diquat required to inhibit oxidationin vivo and its short residual half—life in aquatic environments, as a result of adsorption and non—enzymmatic transformation, the novel interactions demonstrated are probably of little significance under the practical conditions in which diquat is used.