Abstract
Benzoylphenyl ureas such as diflubenzuron and its analogs, are very effective in controlling a broad spectrum of insect pests. This class of chemicals are primarily stomach toxicants of larvae (Wellinga et al. 1973a, b) but are also known to affect adults (Soltani et al. 1984) and eggs (Wright and Spates 1976, Wright and Harris 1976, Fraragalla et al. 1980, Grosscurt 1980). These compounds either disrupt larval development or prevent egg-hatch, presumably by interfering with cuticle deposition (Mulder and Gijswijt 1973, Ishaaya and Casida 1974) and chitin synthesis (Post and Vincent 1973, Post et al. 1974, Deul et al. 1978, Gijswijt et al. 1979). These chitin synthesis inhibiting growth regulators appear to be insect or arthropod specific and have relatively low acute toxic effects on non-target species such as birds, fishes and mammals. Although they are currently being used for crop protection against many pests of economic importance, further studies on the mode of action are necessary to explain the secondary effects that are unrelated to chitin synthesis such as nucleic acid metabolism (Meola and Mayer 1980, DeLoach et al. 1981) and molting hormone metabolism (Yu and Terriere 1975, Schefle and Kuchenmeister 1981, Soltani et al. 1984). In order to understand the mode of action of the benzoylphenyl ureas at the cellular level, we focussed our studies on the efficiency of inhibition of chitin synthesis during cuticle development by diflubenzuron.
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