Metabolic resistance mechanisms of the housefly (Musca domestica) resistant to pyraclofos

In vivo and in vitro metabolism of pyraclofos labeled with 14C on benzene ring was studied in the pyraclofos-resistant and -susceptible female houseflies. In vivo metabolism studies, the metabolic rate of pyraclofos was the same in both strains. Pyraclofos primarily undergoes metabolic detoxification by cleavage of P–S-alkyl bond, and cleavage of the P–O-aryl bond followed by CHP [1-(4-chlorophenyl)-4-hydroxypyrazole]]–glucose conjugation. Cleavage of P–O-aryl bond and CHP–glucose conjugation is more predominant in the resistant strain whereas the cleavage of P–S-propyl bond resulting in EHP–CHP [O-1-(4-chlorophenyl)pyrazol-4-yl ethyl hydrogen phosphate] is more preferred in the susceptible strain. CHP production by P–O-aryl bond cleavage was controlled by P450 monooxygenase and esterase. UDP–glucosyltransferase appeared to play an important role in the pyraclofos metabolism of the resistant strain. Production of CHP–glucose conjugate was largely reduced by piperonyl butoxide and S,S,S-tributylphosphorotrithioate in both strains. EHP–CHP production seemed to be controlled by P450 monooxygenase and stimulated by UDP–glucose.