4.5 Article

Gonadal development and transcript profiling of steroidogenic enzymes in response to 17α-methyltestosterone in the rare minnow Gobiocypris rarus

期刊

出版社

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.jsbmb.2014.03.001

关键词

Steroidogenic genes; 17 alpha-Methyltestosterone; 17 alpha-Ethinylestradiol; Histology; Gobiocypris rarus

资金

  1. National Natural Science Foundation of China [31270547]
  2. Natural Science Foundation of Shaanxi Province, China [2011JM3009]
  3. Fundamental Research Funds for the Central Universities in Northwest AF University [QN2011062]

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It is well known that natural and anthropogenic chemicals interfere with the hormonal system of vertebrate and invertebrate organisms. How these chemicals regulate gonadal steroidogenesis remains to be determined. The main objective of this study was to evaluate the effects of 17 alpha-methyltestosterone (MT), a synthetic model androgen, on gene expression profiles of six key steroidogenic genes in adult rare minnow. The full-length cDNA encoding 11 beta-hydroxysteroid dehydrogenase-2 (11 beta-HSD2) was firstly isolated and characterized by RT-PCR and RACE methods. The gonadal transcript changes of StAR, cyp11a1, 3 beta-HSD, cyp17a1, 11 beta-HSD2 and cyp19a1a in 6-month adult Gobiocypris rams exposed to MT and 17 alpha-ethinylestradiol (EE2) for 7, 14 and 21 days were detected by qRT-PCR. To make an effort to connect the transcriptional changes of steroidogenic enzymes with effects on higher levels of biological organization and on VTG, one remarkable sensitive target of steroids, body and gonad weights, histology of gonads, and hepatic vtg mRNA level were measured. MT caused varying degree of abnormalities in ovaries and testes. The hepatic vtg mRNA level was highly inhibited in females and slightly altered in males by MT. Transcripts of several steroidogenic genes including StAR, cyp17a1, and cyp11a1 showed high responsiveness to MT exposure in G. rams. The gene expression profiles of these steroidogenic genes in MT-treated groups were much distinct with the EE2-treated group. (C) 2014 Elsevier Ltd. All rights reserved.

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