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Anabolic steroids are a class of drugs with a basic steroid ring structure that produces anabolic and androgenic effects, respectively. The two primary components of anabolism are testosterone and dihydrotestosterone (DHT). The first two are derived from the androgen receptor (AR), and the latter is derived from the androstenedione receptor (AR5b). DHT is primarily synthesized from testosterone, but a small amount is also obtained from dihydrotestosterone (DHT dihydrotestosterone). Therefore, androgen receptor activators can enhance androgenic responses. Many of the anabolic steroid compounds in use today are DHT. However, most DHT is converted to androstenedione through the enzyme aromatase (17β-hydroxysteroid dehydrogenase). This enzyme is present in most cell types and is inhibited by some endogenous steroids (8, 9). However, as a result of the recent development of synthetic androgen-receptor-activating enzymes, one can readily and with greater ease produce DHT. Therefore, any one type of a steroid can be easily converted to another type of a steroid in vivo, in order to produce anabolic androgenic effects. Steroid drugs commonly utilized for muscle growth and repair have similar androgenic activity as the the human endogenous estrogen hormone, estradiol. For example, testosterone hydrochloride, a synthetic androgen-receptor activator, is often used to stimulate growth in the prostate gland (10). Inhibition of aromatase in prostate cancer cells leads to decreased breast cancer growth (2). Because aromatase has been inhibited in a variety of prostate cancer cell lines, one of the main uses of synthetic androgens in cancer therapy is to activate this enzyme. However, the same androgen-receptor-activating substances also inhibit aromatase in human breast cancer cells, which may account for the increased breast cancer response to androgens in androgen-receptor-activating drugs than to estrogens (11). Thus, the development of novel androgen-receptor-activating compounds also presents an opportunity to augment the breast carcinogenic androgen response seen with estrogen. Treatment of male pattern baldness In the 1970s and 1980s, anabolic steroid treatment of male pattern hair loss (MPD) was a widespread and popular treatment. This treatment was based on the hypothesis that testosterone deficiency leads to impaired development of hair follicles, and this leads to the development of a baldness phenotype, characterized by thinning of facial follicles, and an increase in hair growth over Similar articles:

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