β-Naphthoflavone alters normal plasma levels of vitellogenin, 17β-estradiol and luteinizing hormone in sea bass broodstock

Abstract

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 β-naphthoflavone (βNF), 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 βNF antagonizes the 17β-estradiol (E2)-mediated production of vitellogenin (VTG) in cultured rainbow trout hepatocytes in vitro. This antiestrogenic effect appeared to be related to the βNF activation of the AhR pathway. The questions addressed in the present study are: (a) if βNF 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 βNF-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 βNF-fed fish indicates that the test compound was accumulated and effective. Compared to the control fish, βNF 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 βNF on VTG synthesis and to an interference with the hypothalamus-pituitary-gonad axis in reproducing sea bass.