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.

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.

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.