Neonicotinoid insecticides and selective serotonin reuptake inhibitors interact antagonistically in Daphnia magna
2019
Schlussel, Adeline | Leininger, Elizabeth
Water pollution caused by increasing pharmaceutical and pesticide use has the potential to negatively affect aquatic ecosystems through the effects of individual chemicals and potentially synergistic mixtures. However, mixtures' synergistic effects are less well understood than the individual effects of their constituents. One mechanism for synergism is enzyme inhibition. The antidepressant fluoxetine inhibits cytochrome P450 enzymes (CYPs) in several taxa, including humans, fish, and polychaetes. CYPs are also used by macroinvertebrates to detoxify neonicotinoid insecticides, which can have detrimental impacts on aquatic macroinvertebrate communities. We hypothesized that fluoxetine inhibits invertebrates' ability to detoxify neonicotinoids, resulting in synergistic toxicity to aquatic macroinvertebrates. Acute (24-hour) immobilization assays with the water flea Daphnia magna were used to assess the toxicity of fluoxetine, the neonicotinoid imidacloprid, and a mixture of the two. Individual dose-response curves revealed an EC₅₀ of 5.43 mg/L for fluoxetine and 10 mg/L for imidacloprid. A fluoxetine/imidacloprid mixture immobilized significantly fewer D. magna than did the individual chemicals, suggesting that these chemicals may interact antagonistically in D. magna. However, mixtures of imidacloprid and prochloraz, a known inhibitor of D. magna CYPs, also exhibited a near-significant antagonistic interaction. These antagonisms could stem from imidacloprid's inhibition of feeding in D. magna or fluoxetine's inhibition of imidacloprid's target receptor. Even if fluoxetine and imidacloprid are not synergistically toxic, they could still individually impact macroinvertebrates. Moreover, diversity in the invertebrate community suggests that research in additional species is warranted.
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