Abstract
Until such time as the receptor protein-hormone complexes are purified to homo geneity and their role in the regulation of biochemical reactions is precisely defined, the foundations of the receptor concept currently rest on impressive, but nevertheless indirect, evidence. However, by judicious use of antagonists of steroid hormones, the mandatory involvement of receptor proteins in the expression of the vast majority of hormonal responses is now established beyond reasonable doubt. Many compounds are able to suppress the biological activity of androgens and may thus be reasonably described as antiandrogens. The two most intensively studied antiandrogens, cyproterone acetate (6α-chloro-17α-acetoxy-1,2α-methylene-4, 6-pregnadien-3, 20-dione) and BOMT (6α-bromo-17α-methyl-17β-hydroxy-4-oxa-5α;-androstan-3-one) are structurally related to steroids. Both counter the formation of receptor protein-5α-dihydro testosterone complex (Fang and Liao, 1969; Mangan and Mainwaring, 1972; 1973), and negate most manifestations of the androgenic response. A wide spectrum of processes is impaired in androgen target cells by antiandrogens, including the induction of enzymes, such as acid phosphatase (Geller et al, 1969) and type A aldolase (Mainwaring et al., 1974 b), ribosomal RNA synthesis, and nucleolar (form A) RNA polymerase activity (Mainwaring et al., 1971), polyribosome synthesis (Mainwaring and Wilce, 1973), poly (A)-rich messenger RNA synthesis (Mainwaring et al., 1974 c), polyamine synthesis (Mangan et al., 1973) and many enzymes engaged in DNA synthesis (Rennie et al., 1975). This comprehensive list indicates the very extensive involvement of the receptor system in the mechanism of action of androgens.
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© 1977 Springer-Verlag New York Inc.
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Mainwaring, W.I.P. (1977). Experimental Support for the Model. In: The Mechanism of Action of Androgens. Monographs on Endocrinology, vol 10. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-88429-0_4
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DOI: https://doi.org/10.1007/978-3-642-88429-0_4
Publisher Name: Springer, Berlin, Heidelberg
Print ISBN: 978-3-642-88431-3
Online ISBN: 978-3-642-88429-0
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