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The same classic androgen receptor can be characterized in the prostate, the bulbocavernosus/levator ani muscle and typical skeletal muscles of the rat (Krieg and Voigt, 1977). Nandrolone (19-nortestosterone) and 5?-DHT have a higher binding affinity than testosterone with the receptor. The prostate has 7 times the concentration of androgen receptors than the bulbocavernosus/levator ani muscles which in turn has 10 times more than other skeletal muscle. In vitro studies by Gloyna and Wilson (1969) and Massa and Martini (1974) have shown that 5?-reductase activity is very high in rat sexual tissue such as the prostate and seminal vesicles but negligible, if at all, in skeletal muscle such as the levator ani and thigh muscle. Intracellular DHT is, therefore, low in skeletal muscle, and it is worth emphasizing that its presence is further diminished because of the high activity of the enzyme 3?-hydroxysteroid-dehydrogenase in this tissue (and cardiac tissue as well), the enzyme that converts DHT irreversibly to 3?-androstanediol (Massa and Martini, 1974; Smith et al. The very low activity of 5?-reductase in skeletal (and cardiac) muscle was subsequently confirmed by other investigators (Krieg et al. The rat levator ani may be a somewhat atypical striated muscle because of its greater concentration of androgen receptors, but, due to its very low 5?-reductase activity, it can also be argued that it is not a typical part of target tissues associated with the reproductive system. Celotti and Cesi (1992), in their review of possible mechanisms of action of anabolic steroids, discuss that the peculiar androgen sensitivity of this muscle is intermediate between that present in the skeletal muscles and that of the prostate. The myotrophic effect of anabolic steroids may be reflected by the amplified response of the levator ani muscle due to its higher concentration of androgen receptors, an effect that is not apparently sufficient in other (typical) rat skeletal muscles to be observed using differences in weight (compared with controls) as the measurand. A possible basis for increasing the myotrophic-to-androgenic ratio may be by exploiting the fundamental difference between the 5?-reductase concentrations in skeletal muscle and androgenic tissue. One way of increasing the anabolic’androgenic dissociation is to administer a steroid that has a greater binding affinity for the androgen receptor but upon reduction to a 5?-metabolite has a lesser affinity. Among the anabolic steroids, 19-nortestosterone (nandrolone) was one of the first synthesized, the most used and probably the best studied. Although DHT has a greater binding affinity for the androgen receptor than its parent steroid testosterone, by contrast the 5?-reduced form of 19-nortestosterone, 5?-dihydro-19-nortestosterone, has a lesser binding affinity than its parent steroid 19-nortestosterone (Toth and Zakar, 1982). Hence, in androgenic tissue, testosterone is converted to a more potent metabolite, whereas 19-nortestosterone is converted to a less potent one. As 5?-reduction occurs readily in androgenic tissue but is negligible in skeletal muscle, this explains why 19-nortestosterone has a greater myotrophic-to-androgenic ratio when compared with testosterone ( Figure 6 ). If the model is correct, such a diminishment in androgenic activity should not be confined to the accessory reproductive tissues in the human such as the prostate, but also in non-genital target tissues where clear roles for the metabolism to DHT have been defined such as the male patterns of facial and body hair growth, thus allowing more muscle per whisker. Moreover, even where testosterone rather than DHT appears to stimulate other secondary sexual characteristics, such as voice deepening, with the discovery of two isozymes of 5?-reductase (for review see Russell and Wilson, 1994), it cannot be ruled out that some of these actions attributed to testosterone need to be re-evaluated, the results of which may have relevance to the applicability of anabolic steroids with a high myotrophic’androgenic index. 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, buy winstrol oral 10 mg oral steroids oral winstrol. 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. In skeletal muscle, 5?-reductase activity is negligible and, therefore, the parent steroid itself binds with strong affinity to the androgen receptor.
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