Various advantages of Drosophila melanogaster in the detection of chemical mutagens have been extensively discussed [7,8]. The capability of Drosophila for metabolic activation of known precarcinogens into active electrophilic forms has been convincingly demonstrated by Vogel [11]. The existence of a mixed-function-oxidase system even in the gonadal tissues of Drosophila [1] enables sensitive detection of short-lived reactive intermediates. Furthermore, it enables the use of various enzyme inducers as well as inhibitors, as in mammalian experiments. Recently the use of sodium phenobarbiturate to induce the cytochrome P-450 system in Drosophila has been described by Magnusson and Ramel [3]. In the present paper we report rather similar results of the exposure of Drosophila to phenobarbitone as a pretreatment to the exposure to styrene and styrene oxide. The use of phenobarbitone results in a further increase in the recessive-lethal frequency after exposure to styrene as well as after styrene oxide. Furthermore, the use of a potent epoxide hydrase inhibitor, trichloro-propane oxide [4], results in a significant rise in recessive lethals during exposure to styrene oxide. © 1979.
