Meeting Abstract
44.10 Jan. 6 Vitellogenin induction by commercial fish food: possible implications in endocrine disruptor studies DAVIS, L.K.; HIRANO, T.; GRAU, E.G.*; Hawaii Institute of Marine Biology, University of Hawaii, Kaneohe lkdavis@hawaii.edu
In a number of teleost fish, male plasma has been found to contain substantial levels of 17&beta-estradiol (E2) and in certain cases, vitellogenin (Vg), a female-specific precursor of egg yolk protein. The presence of E2 and Vg in males raises questions about their etiology and may complicate assessment of environmental endocrine disruptors by masking their effects. In order to examine whether components of commercial fish food might induce Vg production, we measured Vg levels in male tilapia (Oreochromis mossambicus) that were fed either commercial feed, commercial feed treated with E2 (5 &mug/g of feed), or a diet consisting of 50% squid and 50% mixed vegetables. Fish were fed for 40 days and sampled every 10 days. Plasma Vg in fish fed commercial feed remained constant at 3-7 mg/ml, while levels of fish fed E2 significantly increased to 45 mg/ml. Plasma Vg of squid/vegetable-fed fish declined over time to often undetectable levels. Expression of three Vg genes (Vgs A-C) in the liver of squid/vegetable-fed fish, decreased to 0.6 – 3.2% of levels in control fish after 40 days while gene expression of Vgs A-C in E2-fed fish increased by up to 25 fold. In a short term experiment, a single injection of 5 &mug/g E2 increased plasma levels of E2 and Vg within 24 hours. A single injection of a high dose of o,p�-DDE (100 &mug/g) also increased gene expression of Vgs A-C, but did not alter plasma Vg levels. We hypothesize that E2, most likely from the fish meal component of the feed, induces gene expression and production of Vg in male tilapia. Sustained use of this diet will maintain Vg production, a protein with no known function in male fish. Reducing Vg production by feeding an estrogen-free diet may provide a more sensitive and suitable model to assess the effects of environmental endocrine disruptors.
