Transport of androgens in the body

In the periphery steroids equilibrate rapidly between various organs and blood. This fact can be derived from identical levels of free testosterone in saliva and blood (Wang et al. 1981). The total concentrations of steroids in target tissues and body fluids is mainly dependent on the presence of binding proteins such as

Fig. 1.6 Production, transport and metabolism of biologically active androgens.

sex hormone binding globulin (SHBG), and albumin (see Figure 1.6). Binding proteins in body fluids can act as a storage form for steroids that have a high rate of metabolism during passage of blood through the liver (Mendel 1989). In this way, extensive metabolism of active steroids can be inhibited. However, the presence of SHBG and albumin in body fluids is not essential for steroid homeostasis. This can be inferred from analbuminemic rats that possess neither SHBG nor albumin. In these rats, which are fertile, the total plasma concentration of testosterone is much closer to the free concentration in normal rats (Mendel et al. 1989). The free testosterone concentration is within the range of the affinity constant of the androgen receptor Kd 10-9-10-10M. Changes in the peripheral free testosterone concentration can therefore be directly sensed by the androgen receptor if there is equilibration between the exterior and interior of androgen target cells. It is not easy to envisage how steroids such as dihydrotestosterone and 17^-estradiol which can be present in picomolar concentrations (free) can be biologically active when the affinity constants for the receptors are in the (sub)nanomolar range. However, it has become clear that steroid receptors can also be (partly) activated, independent of steroids, by phosphorylation. It is not impossible that such "predisposed receptors" can be activated further by binding very small amounts of steroid (O'Malley et al. 1995). In some cases local production can furnish these active steroids, as for instance dihydrotestosterone in the prostate (Coffey 1988) and 17^-estradiol in the brain (Michael et al. 1986). If the capacity of such local production is sufficiently high, this could explain the apparent discrepancy between receptor affinity and the plasma availability. Alternatively, specific transport systems for steroids into or out of target cells are a possibility, as discussed previously for corticosteroids and their derivatives. Although such transport systems have not been shown to affect the distribution of natural androgens, this may not hold true for synthetic androgenic compounds.

Hair Loss Prevention

Hair Loss Prevention

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