Due to the detection frequencies and measured concentrations
in
surface water, the type I pyrethroid insecticide, bifenthrin, has
been of particular concern within the Sacramento-San Joaquin Delta
in California. Concentrations have been detected above levels previously
reported to impair neuroendocrine function and induce neurotoxicity
to several species of salmonids. Metabolomic and transcriptomic studies
indicated impairment of cellular signaling within the brain of exposed
animals and potential alteration of lipid metabolism. To better understand
the potential impacts of bifenthrin on brain lipids, juvenile rainbow
trout (
Oncorhynchus mykiss
) were exposed
to mean bifenthrin concentrations of 28 or 48 ng/L for 14 days, and
non-targeted lipidomic profiling in the brain was conducted. Brain
tissue sections were also assessed for histopathological insult following
bifenthrin treatment. Bifenthrin-exposed trout had a concentration-dependent
decrease in the relative abundance of triglycerides (TGs) with levels
of phosphatidylcholines (PCs) and phosphatidylethanolamines (PEs)
significantly altered following 48 ng/L bifenthrin exposure. An increased
incidence of histopathological lesions, such as focal hemorrhages
and congestion of blood vessels, was noted in the brains of bifenthrin-treated
animals, suggesting an association between altered lipid metabolism
and neuronal cell structure and integrity.
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