J. Anim Sci.
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Published online first on July 3, 2007
J. Anim Sci. 1990. doi:10.2527/jas.2007-0087
© 2007 American Society of Animal Science

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J. Anim Sci., doi: 10.2527/jas.2007-0087
©Copyright, 2007, The American Society of Animal Science


ARTICLE

Gene expression of 3{beta}-hydroxysteroid dehydrogenase and 17{beta}-hydroxysteroid dehydrogenase in relation to androstenone, testosterone, and estrone sulphate in gonadally-intact male and castrated pigs

G. Chen 1*, E. Bourneuf 2, S. Marklund 2, G. Zamaratskaia 1, A. Madej 3, K. Lundström 1

1 Department of Food Science, Swedish University of Agricultural Sciences, P.O. Box 7051, SE-750 07 Uppsala, Sweden
2 Department of Animal Breeding and Genetics, Swedish University of Agricultural Sciences, Uppsala Biomedical Centre, P.O. Box 597, SE-751 24 Uppsala, Sweden
3 Department of Anatomy, Physiology and Biochemistry, Swedish University of Agricultural Sciences, P.O. Box 7011, SE-750 07 Uppsala, Sweden

* To whom correspondence should be addressed. E-mail: Gang.Chen{at}lmv.slu.se.


   Abstract

Androstenone is one of the main compounds responsible for boar taint and 3{beta}-hydroxysteroid dehydrogenase (3{beta}HSD) might be involved in its metabolism. In this study, the gene expression of 3{beta}HSD and 17{beta}-hydroxysteroid dehydrogenase (17{beta}HSD) were determined by real-time PCR analysis and related to the concentrations of androstenone, testosterone, and estrone sulphate (E1S). The experiments were performed on gonadally-intact male pigs classified based on high or low fat androstenone concentrations as predetermined by HPLC, as well as on immunocastrated and surgically castrated pigs. The pigs with high androstenone concentrations in fat had low 3{beta}HSD gene expression in liver and testis. Moreover, the 17{beta}HSD gene expression in liver, but not in testis, varied negatively with fat androstenone concentrations. Immunocastrated and surgically castrated pigs had nondetectable concentrations of both fat androstenone and plasma testosterone and E1S, and the castration procedure induced a significant increase of 3{beta}HSD and 17{beta}HSD gene expression. The mRNA expression was generally much greater from the 3{beta}HSD than from the 17{beta}HSD gene. Furthermore, fat androstenone was negatively correlated with liver 3{beta}HSD gene expression (Pearson correlation, r = -0.69; P < 0.05), and the 17{beta}HSD gene expression in liver was negatively correlated with plasma E1S (r = -0.95; P < 0.001), indicating an important role of liver 17{beta}HSD in the estrogen metabolism of gonadally-intact male pigs. Another strong correlation was found between 3{beta}HSD and 17{beta}HSD gene expression in liver of the gonadally-intact male pigs (r = 0.86; P < 0.01), possibly reflecting similar regulation mechanisms of these genes.

Key Words: Androstenone, estrone sulphate, 3{beta}-hydroxysteroid dehydrogenase, 17{beta}-hydroxysteroid dehydrogenase, pig, testosterone







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