Mechanisms of parathion resistance in the greenbug, schizaphis graminum (rondani)

Results of studies to determine the mechanism of parathion resistance in greenbugs, Schizaphis graminum (Rondani), indicate that the resistance is due to the combined effects of metabolic detoxification and target site insensitivity. Resistance to parathion is partially suppressible by the hydrolytic enzyme inhibitor DEF, suggesting involvement of hydrolytic enzymes and is in agreement with increased general esterase activity previously observed in the resistant aphids. The large increase in resistance observed in insects pretreated with the mixed function oxidase inhibitor, piperonyl butoxide, may indicate that metabolic factors associated with the resistance are more active toward the phosphorothioate molecule, although increased metabolism of paraoxon may have also resulted in higher resistance levels. In vivo metabolism experiments confirm the involvement of metabolic detoxification in the resistance based on decreased rates of parathion recovery and paraoxon formation in the resistant strain. Resistance was also associated with a 2.5-fold decrease in sensitivity of acetylcholinesterase to paraoxon inhibition and, therefore, target site insensitivity and metabolic detoxification interact to confer overall resistance levels.