DECAMETHRIN METABOLITES FROM OXIDATIVE, HYDROLYTIC, AND CONJUGATIVE REACTIONS IN MICE

Mouse metabolism of orally administered decamethrin differs from previous findings with rats as follows: the feces contain less decamethrin and more monohydroxy and dihydroxyester metabolites; more acid moiety metabolites are hydroxymethyl derivatives and less alcohol moiety metabolites are phenolic compounds: metabolites in mouse but not rat excreta include 3-(2, 2-dibromovinyl)-2-'rans-hydroxymethyl-2-methylcyclopropanecarboxylic acid sulfate, 3-phenoxybenzaldehyde, 3-phenoxybenzyl alcohol and its glucuronide, glucuronides of 4'-hydroxy-3-phenoxybenzyl alcohol and 5-hydroxy-3-phenoxybenzoic acid, and 3-phenoxybenzoyltaurine. Intraperitoneal (ip) administration yields the same metabolites but in different ratios. Decamethrin is hydrolyzed in vitro by esterases in blood, brain, kidney, liver, and stomach preparations. Mice pretreated with piperonyl butoxide (PB) or S, S, S-tributyl phosphorotrithioate (DEF) metabolize decamethrin less readily than normal mice by oxidative or hydrolytic pathways, respectively. Equitoxic doses of decamethrin (twice the LD50, 6-191 mg/kg) administered orally or ip with different vehicles or ip to PB-or DEF-treated animals yield similar levels (-0.5 ppm) of decamethrin in the brain. Severe poisoning symptoms result on introducing this level of decamethrin into the brain by direct injection. © 1979, American Chemical Society. All rights reserved.