Previous studies in euryhaline fish have shown that acclimation to hypersaline environments enhances the toxicity of thioether organophosphate and carbamate pesticides. To better understand the potential mechanism of enhanced toxicity, the effects of the organophosphate insecticide phorate were evaluated in coho salmon (Oncorhynchus kisutch) maintained in freshwater (<0.5 g/L salinity) and 32 g/L salinity. The observed 96-h LC50 in freshwater fish (67.34 ± 3.41 μg/L) was significantly reduced to 2.07 ± 0.16 μg/L in hypersaline-acclimated fish. Because organophosphates often require bioactivation to elicit toxicity through acetylcholinesterase (AChE) inhibition, the in vitro biotransformation of phorate was evaluated in coho salmon maintained in different salinities in liver, gills, and olfactory tissues. Phorate sulfoxide was the predominant metabolite in each tissue but rates of formation diminished in a salinity-dependent manner. In contrast, formation of phorate-oxon (gill; olfactory tissues), phorate sulfone (liver), and phorate-oxon sulfoxide (liver; olfactory tissues) was significantly enhanced in fish acclimated to higher salinities. From previous studies, it was expected that phorate and phorate sulfoxide would be less potent AChE inhibitors than phorate-oxon, with phorate-oxon sulfoxide being the most potent of the compounds tested. This trend was confirmed in this study. In summary, these results suggest that differential expression and/or catalytic activities of Phase I enzymes may be involved to enhance phorate oxidative metabolism and subsequent toxicity of phorate to coho salmon under hypersaline conditions. The outcome may be enhanced fish susceptibility to anticholineterase oxon sulfoxides.
