EFFECT OF PIPERONYL BUTOXIDE ON THE ABSORPTION AND METABOLISM OF CHLORDIMEFORM BY LARVAE OF THE CATTLE TICK, <i>BOOPHILUS MICROPLUS</i>*

Abstract

Abstract Cattle tick larvae continuously exposed to 0.02% N ′‐(4‐chloro‐ o ‐toryi)‐ N , N ‐dimethylformamkline (chlordimeform‐ 14 C) in impregnated packets absorbed the acaricide and metabolized it to N ′‐(4‐chloro‐ o ‐tolyl)‐ N ‐methylformamidine (demethylchlordimeform), 4′‐chloro‐ o ‐formotolutdide, 4‐chloro‐ o ‐toluidine, and an unidentified polar conjugate. Larval mortality was greatest between 24 and 48 h, and more than 85% of larvae were dead by 48 h. During this time interval (24 to 48 h) demethylchlordimeform, itself an acaricide, was the major metabolite. Cattle tick larvae continuously exposed to 0.02% chlordimeform‐ 14 C in the presence of 0.2% piperonyl butoxide absorbed less of the acaricide, metabolized comparatively little of it, and were all still alive at 48 h. Thus piperonyl butoxide blocked the metabolism of chlordimeform probably by inhibiting the mixed function oxidase system responsible for catalyzing the oxidative N‐dealkylation to demethylchlordimeform. The data are consistent with the view that demethylchlordimeform is the lethal toxicant in chlordimeform‐poisoned cattle tick larvae.