Beta-naphthoflavone alters normal plasma levels of vitellogenin, 17 beta-estradiol and luteinizing hormone in sea bass broodstock.

A variety of environmental pollutants exhibit antiestrogenic properties, i.e. these compounds antagonize estrogen-dependent processes in their target tissues. This is the case with beta-naphthoflavone (beta NF), a compound that is known for its ability to bind to the arylhydrocarbon receptor (AhR) and thereby to induce cytochrome P4501A (CYP1A) expression. In previous studies, we have shown that beta NF antagonizes the 17 beta-estradiol (E2)-mediated production of vitellogenin (VTG) in cultured rainbow trout hepatocytes in vitro. This antiestrogenic effect appeared to be related to the beta NF activation of the AhR pathway. The questions addressed in the present study are: (a) if beta NF is able to evoke an antiestrogenic effect in fish in vivo; this was estimated from circulating VTG levels, and (b) if the antiestrogenic action is expressed not only at the cellular (suppressed VTG synthesis) but also at the systemic level; this was addressed by measuring the circulating level of two hormones directly implicated in the regulation of reproductive processes: E2 and luteinizing hormone (LH). As experimental model, we used broodstock sea bass (Dicentrarchus labrax). The fish were fed with a beta NF-enriched diet from December, at the beginning of the reproductive period of sea bass, until the termination of this period in April. Induction of hepatic 7-ethoxyresorufin-O-deethylase (EROD) activity and CYP1A mRNA levels in beta NF-fed fish indicates that the test compound was accumulated and effective. Compared to the control fish, beta NF treatment of sea bass was associated with a significant reduction of plasma VTG levels, and it disturbed the reproduction-related fluctuations of plasma E2 and LH levels. These findings point to an antiestrogenic effect of beta NF on VTG synthesis and to an interference with the hypothalamus-pituitary-gonad axis in reproducing sea bass.