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With these, the field of medicine has sought to obtain the anabolic effect of testosterone without its virilizing adverse effects so that women and children could use anabolic steroids as wellas males. Testosterone (T) is chemically synthesized by the adrenal cortex of the human adrenal gland and converted into binding and active forms by the enzyme 5-adenosine arabinoside-3 acetyltransferase (5-ARDAT).1, 2 It may only be synthesized in the testicles of a select group of animals, but there is no proof of selective production by the germ cells of the testicles of humans.3-5
The synthesis of T, the conversion of T into its active and binding forms, and the biosynthesis or biosynthetic pathways for all the biosynthetic and non-BMI related active hormones (DHEA, DHEAS, and others) can be used to identify the species that can convert testosterone into DHEA and its primary metabolite DHEA-S, DHEAS. The biosynthetic pathways for all of these metabolites have also been determined and this information combined with the known and expected non-BMI related biosynthetic pathways for DHEA, DHEAS and possibly testosterone, can be used to identify the species that can convert testosterone into DHEA and its primary metabolite DHEA-S, DHEAS. We know from genetic studies that humans have a polymorphism of the 5-ARDAT gene (known as 5-ADOR CT genotype) which results in a higher than normal conversion rate of DHEA into DHEAS.6, 7
When testosterone is synthesized from 5-ARDAT, it is converted into more than two and even three additional molecules. These additional molecules then are converted back to an inactive inactive T and are converted back to testosterone, in this way the ratio of total testosterone to DHT may vary by 0.3:1 in humans (a ratio greater than 1, which is more common in males, is abnormal and the ratio should be >1.0).8
When DHEA and DHEAS are synthesized from T, many of the molecules in DHEA and its main metabolite DHEAS are also produced after T is formed and thus T may be a source for DHEA and its primary metabolite DHEA-S.9
Although these two studies did not consider the possible conversion of testosterone into allosteric modulators, this conversion may very well be a significant source for the testosterone-derived compounds and metabolites discussed above.
The 5-ARAT gene polymorphism can affect the
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