Bifenthrin is a pyrethroid insecticide used in urban and agricultural applications. Previous studies have shown that environmentally relevant (ng/L) concentrations of bifenthrin increased plasma concentrations of 17b-estradiol (E2) and altered the expression of dopaminergic pathway components. The dopaminergic neurons can indirectly regulate E2 biosynthesis, suggesting that bifenthrin may disrupt the hypothalamic-pituitary-gonadal (HPG) axis. Because embryos do not have a complete HPG axis, the hypothesis that bifenthrin impairs dopamine regulation was tested in embryonic and 1-mo-old juvenile zebrafish (Danio rerio) with exposure to measured concentrations of 0.34 and 3.1 mg/L bifenthrin for 96 h. Quantitative reverse transcriptase polymerase chain reaction was used to investigate transcripts of tyrosine hydroxylase (TH), dopamine receptor 1 (DR1) and 2A (DR2A), dopamine active transporter (DAT), estrogen receptor a (ERa), ERb1, ERb2, luteinizing hormone b (LHb), follicle-stimulating hormone b (FSHb), vitellogenin (VTG), cytochrome P450 cyp19a1a, and cyp19a1b. Levels of E2 were measured by enzyme-linked immunosorbent assay (ELISA). Dopamine and its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) concentrations were measured by liquid chromatrography-tandem mass spectrometry (LC-MS/MS). Significant decreases in TH and DR1 transcripts and HVA levels, as well as ratios of HVA/dopamine and HVAþDOPAC/dopamine, in zebrafish embryos were observed after bifenthrin treatment. In juveniles, a significant increase in the expression of ERb1 and the DOPAC to dopamine ratio was noted. These results show a possible antiestrogenic effect of bifenthrin in embryos, and estrogenicity in juveniles, indicating life-stage-dependent toxicity in developing fish. Environ Toxicol Chem 2018;37:236-246. C 2017 SETAC

The dopaminergic effect of PAH and PFAS mixtures, prepared based on environmental levels has been studied in juvenile female Atlantic cod (Gadus morhua). Benzo[a]pyrene, dibenzothiophene, fluorene, naphthalene, phenanthrene and pyrene were used to prepare a PAH mixture, while PFNA, PFOA, PFOS and PFTrA were used to prepare PFAS mixture. Cod were injected intraperitoneally twice, with either a low (1x) or high dose (20x) of each compound mixture or various combinations. After two week of exposure, levels of plasma 17β-estradiol (E2) were significantly high in high PAH/high PFAS treated groups. Dopamine: metabolite ratios (DOPAC/dopamine and HVA+DOPAC/dopamine) in brain homogenate changes with the levels of E2 in plasma except for high PAH/low PFAS and low PAH/high PFAS treated groups. In general, th mRNA levels inversely correlated with dopamine: metabolite ratios and gnrh2 mRNA levels. Respective decreases and increases of dr1 and dr2a after exposure to the high PAH dose were observed. Whereas, high PFAS exposure decreased both drs, leading to high plasma E2 concentrations. Other investigated endpoints suggest that these compounds at different doses and combinations have different toxicity threshold and mode of actions. These effects indicate potential alternations in feedback signalling processes within dopaminergic pathway by these contaminants.

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