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Much of the knowledge of the separate roles of testosterone and DHT came from 5?-reductase deficiency syndrome, but these effects are all ascribed to mutations in the type 2 isoenzyme (Randall, 1994) and the biological role of the 5?-reductase type 1 is harder to ascertain as there is no recognized type 1 deficiency. For example, type 2 5?-reductase appears not to be necessary for the sebaceous gland response to androgens and the development of acne, but it is now known that the principal isoenzyme in this gland is the type 1 form (Thiboutot et al. As an adjunct, dutasteride (Avodart; manufactured by GlaxoSmithKline), which inhibits both type 1 and type 2 5?-reductases and is used in the treatment of benign prostatic hyperplasia (Clark et al. This suggests that further work at the molecular level is required to better understand the action of androgens on sebaceous gland function. In androgenic tissues, nandrolone (19-nortestosterone) is readily converted by the enzyme 5?-reductase into 5?-dihydro-19-nortestosterone, i. This metabolite binds with weaker affinity to the androgen receptor compared with the parent steroid. Further metabolism can occur because of the high activity of the enzyme 3-hydroxysteroid-dehydrogenase (which reduces the 3-oxo group) in androgenic tissue., gp stan 50 mg injectable steroids winstrol depot. In skeletal muscle, 5?-reductase activity is negligible and, therefore, the parent steroid itself binds with strong affinity to the androgen receptor. It follows that there is a favourable disassociation of the myotrophic effects from the androgenic effects of nandrolone and also that there is a greater myotrophic-to-androgenic ratio when compared with testosterone. This mechanism of myotrophic’androgenic dissociation does not explain why other anabolic steroids that do not undergo 5?-reduction, for example, those with an extra double bond in the A-ring, such as chlorodehydromethyltestosterone and methandienone (Schanzer, 1996), have a favourable mytotrophic’androgenic index. Even so, it is possible that that myotrophic’androgenic dissociation may occur, simply because the effect of the particular steroid cannot be amplified by 5?-reduction in androgenic target tissues, in common with the hypothesis proposed for the differential action of a steroidal SARM (see the section ‘Selective androgen receptor modulators’ for an explanation of the term) called MENT (7?-methyl-19-nortestosterone; trestolone) (Agarwal and Monder, 1988; Kumar et al. Recently, as part of investigations to assess whether the designer steroid THG had anabolic and androgenic properties (see also next section), three papers report the effects of its administration on the growth of the levator ani, prostate and seminal vesicles compared with control steroids (Jasuja et al. Notwithstanding the possible differences in pharmacokinetics and bioavailability between THG and the control steroids administered, there appeared to be little myotrophic’androgenic dissociation, but, nonetheless, the bioassays clearly demonstrated that THG had anabolic and androgenic activity in vivo , and, therefore, belonged within the banned doping class of anabolic agents in sport, as defined by WADA. As a final and very important point, it is of note that complete dissociation has not been achieved with any anabolic steroid synthesized, and, therefore, the chronic administration of these drugs, even those with a very high myotrophic’androgenic index value, such as found with nandrolone (19-nortestosterone), will result in hirsutism and, eventually, virilization of women and children. Androgen receptor expression and the importance of coregulators. The androgen receptor belongs to the family of nuclear receptor superfamily (Mangelsdorf et al. A DNA-binding domain, a ligand-binding domain and at least two transcriptional activation domains, characterize these receptors. Apart from binding with the steroid, the ligand-binding domain also functions in dimer formation and mediates transcriptional activation. The DNA-binding domain targets the receptor to specific DNA sequences known as steroid (or hormone) response elements. On the receptor, the DNA-binding domain consists of two subdomains called ‘zinc-fingers’; each subdomain contains four cysteine residues that coordinate with a zinc atom, thus, stabilizing the ‘finger’ structure. The zinc-fingers are inserted between specific grooves of the DNA helix, thus, allowing maintenance of DNA-binding activity. A general model of steroid receptor action is displayed in Figure 7. In the absence of hormone, it is by and large accepted that steroid receptors exist as an inactive oligomeric complex, being sequestered by the heat-shock protein (Hsp), Hsp90, which acts as a molecular chaperone. Hsps are so-called because they were discovered to accumulate under stress conditions including within heat-traumatized cells, but many are present and functionally important under normal conditions; they are named according to their molecular weight in kilodaltons. Another chaperone called p23 stabilizes the aporeceptor complex by blocking Hsp90 in the ATP-bound substrate conformation.
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