LAUSR

Sediment contamination can pose risks to the environment, and sediment toxicity tests have been developed to isolate the impact of sediment from other factors. Mixtures of contaminants often occur in sediments, and traditional endpoints used in toxicity testing, such as growth, reproduction, and survival, cannot discern the cause of toxicity from chemical mixtures because of complex interactions. In urban waterways, the synthetic pyrethroid bifenthrin and the metal copper are commonly found in mixtures, so the present study was designed to investigate how these contaminants cause toxicity in mixtures. To investigate this, Chironomus tepperi was exposed to environmentally relevant concentrations of copper and bifenthrin-spiked sediments in a 2-way factorial mixture for 5 d. Growth and expression profiles of cysteine metabolism genes were measured after exposure. Growth increased at low copper concentrations, decreased at high copper concentrations, and was unaffected by bifenthrin exposures. Copper exposures induced possible cellular repair by upregulating S-adenosylmethionine synthetase expression and downregulating expression of S-adenosylhomocysteine hydrolase and cystathionine-β-synthase. Metallothionein upregulation was also observed. Bifenthrin exposure altered cysteine metabolism to a lesser extent, downregulating cystathionine-β-synthase and γ-glutamylcysteine synthase. Synergistic, antagonistic, and dose-dependent interactions were observed, and there was evidence of conflicting modes of action and limited substrate production. These findings demonstrate how contextual gene expression changes can be sensitive and specific identifiers of toxicant exposure in mixtures. Environ Toxicol Chem 2017;36:691-698. © 2016 SETAC.