Abstract Over the past two decades a number of antifungal imidazole and triazole derivatives have been approved for use in agricultural applications. In a recent survey of pesticide concentrations in aquatic ecosystems of Central America, the antifungal triazole compound propiconazole was found to be the most widely distributed pesticide. The technical-grade formulation of propiconazole (TGP) has been shown to induce cytochrome P450 expression in mammalian, avian, and piscine species. In addition, concurrent treatment with technical-grade penconazole and an organophosphate (OP) insecticide has been shown to enhance the acute toxicity of OP insecticides to mammalian and avian species. This enhancement was hypothesized to result from induction of a cytochrome P450-catalyzed reaction(s) that was responsible for activating parent OP insecticides to their toxic oxon metabolite. The present study was conducted to determine if pre-exposure to TGP would enhance the acute toxicity of the OP insecticide parathion to an aquatic species. Pre-exposure to TGP enhanced the acute toxicity of parathion to fathead minnows ( Pimphales promelas). In vitro, TGP-treated hepatic microsomes isolated from fathead minnows had an increased parathion activation rate to paraoxon. An increased parathion activation rate may have been the mechanism responsible for enhancing parathion toxicity. Since TGP is concurrently applied with OP insecticides, the acute toxicity of OP insecticides to non-target organisms may be enhanced by previous exposure to TGP.