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Changes in the relative expression pattern of multiple vitellogenin genes in adult male and larval zebrafish exposed to exogenous estrogens

Production of the lipoprotein vitellogenin (Vg) is induced in fish upon exposure to estrogens and is a biomarker of endocrine disruption in fish. In some fish, three types of Vg (VgA, VgB, and VgC) are recognized and transcribed from at least three distinct Vg genes ( vtg). We investigated expressio...

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Bibliographic Details
Published in:Comparative biochemistry and physiology. Part A, Molecular & integrative physiology Molecular & integrative physiology, 2009-09, Vol.154 (1), p.119-126
Main Authors: Henry, T.B., McPherson, J.T., Rogers, E.D., Heah, T.P., Hawkins, S.A., Layton, A.C., Sayler, G.S.
Format: Article
Language:English
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Summary:Production of the lipoprotein vitellogenin (Vg) is induced in fish upon exposure to estrogens and is a biomarker of endocrine disruption in fish. In some fish, three types of Vg (VgA, VgB, and VgC) are recognized and transcribed from at least three distinct Vg genes ( vtg). We investigated expression of vtg coding for Vg1A/B, Vg2A/B, and VgC in adult male and larval zebrafish exposed to various estrogenic substances. Quantitative PCR was conducted for transcripts of each vtg and a control gene ( β-actin). Male fish were exposed to 17β-estradiol (E2) and 17α-ethinylestradiol, total RNA was extracted from excised liver, and histopathology of liver, trunk kidney, and gonads was conducted. Larval fish were exposed to 10 different estrogenic substances and total RNA was extracted from groups of whole larvae. In adult male fish, the relative fold change varied, but pattern of expression change (i.e., Vg1A/B > Vg2A/B > VgC) was consistent. Larger males exposed to E2 had significantly higher induction of each vtg. In larval zebrafish, the relative fold change in vtg expression varied according to specific estrogenic substance tested, but the pattern of change (i.e., Vg2A/B > Vg1A/B > VgC) was consistent for each substance that induced vtg.
ISSN:1095-6433
1531-4332
DOI:10.1016/j.cbpa.2009.05.009