Toxicity and neurophysiological effects of fipronil and its oxidative sulfone metabolite on European corn borer larvae (Lepidoptera : Crambidae)

The phenylpyrazole insecticide fipronil is the first compound of its class to be registered for commercial use. The mode of action of this class of in secticides involves antagonism of the inhibitory neurotransmitter, gamma -a minobutyric acid (GABA). The sulfone metabolite of fipronil has been report ed to be similar in toxicity to the parent compound. In this study, the tox icity and neurophysiological effects of fipronil and the sulfone metabolite were determined for European corn borer larvae. Fipronil was very toxic to neonate European corn borer larvae in feeding bioassays (LC50 = 334 ng a.i ./cm(2) of treated diet) and to fifth instars in topical bioassays (LD50 18 .78 ng/insect). The sulfone metabolite was slightly more toxic to neonate l arvae (LC50 = 1.44 ng a.i./cm(2)) and equally toxic to fifth instar larvae (LD50 = 19.54 ng/insect) compared with the parent compound. Neonate larvae preexposed to piperonyl butoxide (PBO) residues coated on the inside of gla ss scintillation vials for 6 h at 100 mug/vial resulted in significant anta gonism of fipronil toxicity (LC50 4.39 ng a.i./cm(2)), whereas preexposure to PBO at 1 mug/vial had no effect (LC50 = 2.91 ng a.i./cm(2)). Fifth insta rs topically treated with 10 mug of PBO caused significant antagonism of fi pronil toxicity (LD50 = 34.41 ng/insect). Electrophysiological recordings o f spontaneous electrical activity were conducted on isolated ventral nerve cords from fifth instar larvae. Results from these experiments indicate tha t fipronil and its sulfone metabolite both reverse the inhibitory effect of GABA on spontaneous electrical activity. Fipronil, however, caused an incr ease in spontaneous electrical activity relative to that of the sulfone met abolite.