Chronic nitrate exposure alters reproductive physiology in fathead minnows.

Nitrate is a ubiquitous aquatic pollutant that is commonly associated with eutrophication and dead zones in estuaries around the world. At high concentrations nitrate is toxic to aquatic life but at environmental concentrations it has also been purported as an endocrine disruptor in fish. To investigate the potential for nitrate to cause endocrine disruption in fish, we conducted a lifecycle study with fathead minnows (Pimephales promelas) exposed to nitrate (0, 11.3, and 56.5 mg/L (total nitrate-nitrogen (NO3-N)) from <24 h post hatch to sexual maturity (209 days). Body mass, condition factor, gonadal somatic index (GSI), incidence of intersex, and vitellogenin induction were determined in mature male and female fish and plasma 11-keto testosterone (11-KT) was measured in males only. In nitrate-exposed males both 11-KT and vitellogenin were significantly induced when compared with controls. No significant differences occurred for body mass, condition factor, or GSI among males and intersex was not observed in any of the nitrate treatments. Nitrate-exposed females also had significant increases in vitellogenin compared to controls but no significant differences for mass, condition factor, or GSI were observed in nitrate exposed groups. Estradiol was used as a positive control for vitellogenin induction. Our findings suggest that environmentally relevant nitrate levels may disrupt steroid hormone synthesis and/or metabolism in male and female fish and may have implications for fish reproduction, watershed management, and regulation of nutrient pollution.

Assessment of the toxicological interaction of sertraline with cholinesterase inhibiting insecticides in aquatic insects using the black fly, Simulium vittatum IS-7.

Sertraline is a selective serotonin reuptake inhibitor (SSRI) prescribed as an antidepressant. Although SSRIs are known to block serotonin reuptake sites on cell membranes, they also have been shown to inhibit acetylcholinesterase (AChE) activity. Thus, the interaction of these chemicals with other AChE inhibitors, namely, organophosphate and carbamate insecticides, is of interest. In addition, these insecticides have been shown to interact with serotonergic neuronal pathways creating questions as to how these chemicals might interact. In this study, the interactive effect of sertraline (SSRI) in binary combinations with carbaryl (carbamate insecticide) and diazinon (organophosphate insecticide) was assessed using a 48-h acute toxicity test with black fly larvae, Simulium vittatum IS-7. Results showed that observed mortality was bracketed by the independent action model and concentration addition model with the independent action model slightly underestimating mortality and the concentration addition model slightly overestimating mortality. Varying the concentration of the chemicals in the mixture did not indicate that sertraline was interacting with the insecticides to make them more toxic or vice versa. These results indicate that sertraline and the insecticides are likely eliciting toxicity at separate neuronal pathways since no interaction was observed.

Mechanistic approach to understanding the toxicity of the azole fungicide triadimefon to a nontarget aquatic insect and implications for exposure assessment.

Mechanistic and stereoselective based in vitro metabolism assays were utlilized to gain insight into the toxic mode of action of the 1,2,4-triazole fungicide, triadimefon, with black fly (Diptera: Simuliidae) larvae. Based on results from enzyme inhibitor studies, the metabolism of triadimefon in black fly larvae microsomes was found to occur predominantly via an oxidative P450-mediated pathway; triadimenol was formed via the stereoselective reduction of the prochiral carbonyl group of triadimefon. The relatively minor contribution of carbonyl reduction suggests that triadimefon may inhibit ecdysone 20-monooxygenase and disrupt insect molting hormone biosynthesis. 48-h LC50 tests for triadimefon and triadimenol with black fly larvae yielded median values (with 95% confidence intervals) of 6.1 (5.8-6.4) and 22.3 (20.3-24.1) mg/L respectively. The exposure of black fly larvae to sublethal concentrations of triadimefon resulted in increased microsomal P450 activity and affected the microsomal rates of both triadimefon depletion and triadimenol formation. In contrast to trout, black fly larvae produced a higher fraction of the more toxic triadimenol stereoisomers, which may explain in part why triadimefon exhibited a significantly greater toxicity with black fly larvae than trout. These results illustrate that while LC50 tests conducted with commercial triadimenol would presumably expose each organism to the same relative abundance of the four triadimenol stereoisomers, LC50 tests with triadimefon ultimately expose each organism to a unique set of triadimenol stereoisomers depending upon the organism's stereoselective metabolism.