Abstract

Prothiophos oxon or its S-alkyl homologs(alkyl: methyl, ethyl and butyl) was incubated with a mixture of rat liver microsome and cytosol at 37 °C for 30 min in the following conditions: (a) without NADPH and GSH, (b) with NADPH (condition for sulfoxide formation) and (c) with both NADPH and GSH. Each reaction mixture was lyophilized after adding sucrose and fed to adult female houseflies (susceptible Takatsuki strain). Their mortality was observed at intervals until 48 hr. Dose for each compound was adjusted based on its LD50 value so that the time required for the residual oxon to exert its insecticidal activity was delayed. In the case of S-methyl compound, the mortality in (c) was similar to that in (a), although the remaining oxon in (c) was about half of that in (a). This suggests that the insecticidal effect in (c) may also have been given by something other than the oxon. The mortality in (c) was also higher than that in (b), although the amount of the remaining oxon was the same. Considering the unstability of the sulfoxide formed in the reaction mixture in (b), something stabilized in (c) may have contributed to the insecticidal activity. Without cytosol, the mortality in (c) decreased. The similar tendency was observed with other compounds. When bovine erythrocyte AChE was added to the above incubation mixture, the AChE was inhibited by the reaction mixture strongly in (c) and when more GSH was added regardless of the S-alkyl groups used. The reaction mixture was given to susceptible and resistant (higher glutathione S-transferase activity) strains. The death started later in the resistant strain than in the susceptible strain in (a), but was accelerated in (c) and the period of high mortality was longer in (c) than in (a). The mortality was different between (a) and (c) only during the initial period in the susceptible strain. The above result is well explained by postulating that S-alkyl phosphorothiolate compounds produce sulfoxide that inhibit AChE, while the sulfoxide give another active intermediates conjugated by the GSH-glutathione S-transferase system that also inhibit AChE. These two actions combined are to give an insecticidal effect.

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