Effects of salinity acclimation on the endocrine disruption and acute toxicity of bifenthrin in freshwater and euryhaline strains of Oncorhynchus mykiss

Abstract

The pyrethroid insecticide bifenthrin is frequently detected at ng/L concentrations in tributaries of the San Francisco Bay Delta. The estuary is also experiencing increasing salinity through climate change and water redirection. To evaluate the impacts of hypersaline conditions on bifenthrin toxicity in anadromous salmonids of the San Francisco Bay Delta (CA, USA), a 14-d laboratory exposure was performed using 2 strains of Oncorhynchus mykiss (rainbow trout and steelhead) acclimated to freshwater and to 8 g/L and 17 g/L salinity. The fish were then exposed to nominal concentrations of 0 μg/L, 0.1 μg/L, and 1.5 μg/L bifenthrin. Rainbow trout exhibited significant mortality following exposure to 1.5 μg/L (1.07 ± 0.35 μg/L measured) bifenthrin in freshwater. Elevated levels of Na+/K+ adenosine triphosphatase α1A mRNA subunit expression was observed in the gill of rainbow trout acclimated to hypersaline conditions relative to freshwater animals. No significant difference was noted in Na+/K+ adenosine triphosphatase subunit levels in brains of either strain in freshwater or hypersaline conditions. Likewise, significant differences were not observed in plasma vitellogenin or steroid hormone concentrations in either strain whether maintained in freshwater or saltwater. Saltwater acclimation significantly reduced nicotinamide adenine dinucleotide phosphate–catalyzed biotransformation of bifenthrin in liver microsomes of rainbow trout but not of steelhead. The present study showed that, relative to steelhead, rainbow trout have different responses to bifenthrin acute toxicity as well as different rates of hepatic bifenthrin biotransformation and regulation of Na+/K+ adenosine triphosphatase subunits in gills. These data indicate that significant differences exist between the strains and that animal life history may have important effects on the susceptibility of each strain to environmental contaminants.

Salinity impacts on water solubility and n‐octanol/water partition coefficients of selected pesticides and oil constituents

“…The C1‐DBT and C4‐DBT in both media were estimated to be toxic using the measured log K OW values. Bifenthrins were estimated to be nontoxic in this investigation; however, they have been reported to be toxic in seawater in the literature . A plausible explanation may be the lower salt content in previous research compared with the present investigation (0.8–1.7% vs 3.2%), which may suggest that higher bioavailability for bifenthrin also results in increased toxicity in aquatic organisms.…”

Differential Gene Expression in Liver, Gill, and Olfactory Rosettes of Coho Salmon (Oncorhynchus kisutch) After Acclimation to Salinity

“…Atp1a1 encodes an alpha 1 subunit; the alpha subunit is encoded by multiple genes (reviewed in Kaplan 2002). Upregulation of atp1a1 in the gill is consistent with previous studies, as an increase in activity of gill sodium/potassium ATPases has been used in previous studies as a molecular indicator of smoltification (D’cotta et al 1996; Yada et al 2008; Riar et al 2013). Evan and Somero (2008) reported a 1.6-fold increase in the alpha subunit of Na + /K + ATPase mRNA during 12 h of hyperosmotic stress of Gillichthys mirabilis .…”

Effects of pyrethroid insecticides in urban runoff on Chinook salmon, steelhead trout, and their invertebrate prey

“…Given the general decline of Pacific salmonid populations in California and other western US states over recent decades , pyrethroids entering the American River via urban runoff would be of paramount concern should they be adversely impacting the Chinook salmon and steelhead trout that utilize the river as spawning and/or rearing habitat. Direct toxicity to either salmonid species was not observed in any storm event, and seems unlikely given the results of laboratory studies conducted with steelhead trout, rainbow trout , and Chinook salmon (N. Riar, 2012, Master's thesis, University of California, Riverside, CA, USA). No mortality was seen in steelhead exposed to bifenthrin for 96 h up to 665 ± 174 ng/L or to Chinook salmon up to 490 ± 36 ng/L.…”

“…were < 1 ng/L following 14‐d exposures . In contrast, treatment of steelhead and rainbow trout with 30 ± 16 ng/L, and 25 ± 41 ng/L, failed to induce a similar oocyte precursor protein, Vtg, or plasma sex steroids . Choriogenin has been shown to be a more sensitive indicator than Vtg for estrogen receptor activation , but without knowing antibody titers for the ELISAs that were used in the Menidia and Oncoryhnchus studies, it is difficult to make comparisons between species and assays.…”

“…No mortality was seen in steelhead exposed to bifenthrin for 96 h up to 665 AE 174 ng/L or to Chinook salmon up to 490 AE 36 ng/L. After a 2-wk exposure, no significant mortality was observed in either steelhead or rainbow trout exposed to 30 AE 16 ng/L, and 25 AE 41ng/L, respectively [14]. In comparison, the highest concentration we observed in the river was 14.6 ng/L, and concentrations of this magnitude did not last more than 1 d.…”