Abstract
Diafenthiuron possessed moderate toxicity to adult diamondback moths, Plutella Xylostella (L.) (LD50 269.4 μg/g), low toxicity to twospotted spider mites, Tetranychus urticae Koch (41.7% mortality at 500 ppm), and was inactive against bulb mites, Rhizoglyphus echinopus (Fumouze and Robin) (0% mortality at 1,000 ppm). However, 3-(2,6-diisopropyl)-4-phenoxyphenyl)-1- tert -butylcarbodiimide (DFCD), a diafenthiuron photodegradation product, was highly toxic to diamondback moths (LD50 29.7 μg/g), twospotted spider mites (LC50 8.9 ppm), and bulb mites (LC50 106.6 ppm). The toxicity of diafenthiuron to diamondback moths was antagonized by the mixed function oxidase inhibitor piperonyl butoxide, but the toxicity of DFCD was unaffected by the same treatment. Moreover, bulb mites converted diafenthiuron-14C to DFCD and to 3-(2,6-diisopropyl-4-phenoxyphenyl)-1- tert -butylurea, which was nontoxic. Symptoms in moths treated with diafenthiuron or DFCD were time and dose dependent. These symptoms appeared earlier and with greater intensity in moths treated with the carbodiimide. Symptoms included hyperreflexia and marked hyperactivity manifested chiefly by jumping, increased movement of antennae and mouthparts, spinning, and wing flutter. They were strikingly similar to those manifested by moths treated with N’-(4-chloro- o -tolyl)-N-methylformamidine, a known octopaminergic agonist, and markedly different from symptoms displayed by moths treated with dicyclohexylcarbodiimide and with insecticides and acaricides known to attack cholinergic, GABA-ergic, and other systems. These data suggest that diafenthiuron is a propesticide with lethal action in insects and mites that depends on the carbodiimide metabolite. This metabolite functions as a neurotoxicant, possibly by interfering with a biogenic amine (octopamine) mediated mechanism(s).

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