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In vivo modulation of 17 beta-estradiol-induced vitellogenin synthesis and estrogen receptor in rainbow trout (Oncorhynchus mykiss) liver cells by beta-naphthoflavone.

Vitellogenesis or egg yolk production represents a key estrogen initiated process in oviparous vertebrates which is crucial for oocyte maturation. Previous in vitro studies have shown that cytochrome P4501A1 (CYP1A1)-inducing compounds such as beta-naphthoflavone (betaNF) modulate 17 beta-estradiol-induced vitellogenin (Vg) synthesis in primary cultures of juvenile rainbow trout liver cells. In this study, treatment of juvenile trout with 0.5 mg/kg 17 beta-estradiol plus either 25 or 50 mg/kg betaNF confirmed in vivo that betaNF may depress Vg synthesis by the liver. Alternatively, trout treated with 0.5 mg/kg 17 beta-estradiol plus 12.5 mg/kg betaNF or 5 mg/kg 17 beta-estradiol plus 12.5, 25, or 50 mg/kg betaNF showed a potentiation of Vg synthesis relative to estradiol-only injected fish. These results are significant as they suggest that changing plasma estrogen levels in sexually maturing trout will determine whether or not CYP1A1-inducing compounds may suppress, have no effect, or potentiate estrogen-induced liver Vg synthesis. Depressed Vg synthesis by trout injected with 0.5 mg/kg 17 beta-estradiol plus 50 mg/kg of betaNF correlated with depressed estrogen-binding capacity of liver, as assessed by [3H]17 beta-estradiol binding to liver nuclear protein extracts. Using gel mobility shift assay, the decrease in estrogen responsiveness of liver was not attributed to depressed estrogen response element-estrogen receptor binding. The fish liver vitellogenesis process offers a comparative model with which to further study the mechanism(s) of aryl hydrocarbon receptor-mediated antiestrogenicity and endocrine disruption.