Testosterone Facts And Information - What Is Testosterone?
Testosterone is a steroid hormone from the androgen group. Testosterone is primarily secreted in the testes of males and the ovaries of females although small amounts are secreted by the adrenal glands. It is the principal male sex hormone and an anabolic steroid. In both males and females, it plays key roles in health and well-being. Examples include enhanced libido, energy, immune function, and protection against osteoporosis. On average, the adult male body produces about twenty to thirty times the amount of testosterone that an adult female's body does.
Like other steroid hormones, testosterone is derived from cholesterol. The largest amounts of testosterone are produced by the testes in men, but it is also synthesized in smaller quantities in women by the thecal cells of the ovaries, by the placenta, as well as by the zona reticularis of the adrenal cortex in both sexes.
In the testes, testosterone is produced by the Leydig cells. The male generative glands also contain Sertoli cells which require testosterone for spermatogenesis. Like most hormones, testosterone is supplied to target tissues in the blood where much of it is transported bound to a specific plasma protein, sex hormone binding globulin (SHBG).
Testicular action was linked to circulating blood fractions - now understood to be a family of androgenic hormones - in the early work on castration and testicular transplantation in fowl by Arnold Bethold (1803-1861). Research on the action of testosterone received a brief boost in 1889, when the Harvard professor Charles-Edouard Brown-Séquard (1817-1894), then in Paris, self-injected subcutaneously a “rejuvenating elixir” consisting of an extract of dog and guinea pig testicle. He reported in The Lancet that his vigor and feeling of wellbeing were markedly restored but, predictably, the effects were transient (and likely based on placebo), and Brown-Séquard’s hopes for the compound were dashed. Suffering the ridicule of his colleagues, work on the mechanisms and effects of androgens in human beings was abandoned by Brown-Séquard and succeeding generations of biochemists for nearly 40 years.
The trail remained cold until the University of Chicago’s Professor of Physiologic Chemistry, Fred C. Koch, established easy access to a large source of bovine testicles - the Chicago stockyards – and to students willing to endure the ceaseless toil of extracting their isolates. In 1927, Koch and his student, Lemuel McGee, derived 20mg of a substance from a supply of 40 pounds of bull testicles that, when administered to castrated roosters, pigs and rats, remasculinized them (Gallagher & Koch, 1929). The group of Emil Laquer at the University of Amsterdam purified testosterone from bovine testicles in a similar manner in 1934, but isolation of the hormone from animal tissues in amounts permitting serious study in humans was clearly not feasible until three European pharmaceutical giants –Schering (Berlin, Germany), Organon (Oss, Netherlands) and Ciba (Basel, Switzerland) – began full-scale steroid research and development programs in the 1930’s. Schering’s Adolf Butenandt (1903-1995) worked out the structure of testosterone, and its independent partial-synthesis from a cholesterol base in 1935 by both Butenandt and Leopold Ruzicka (1887-1976) in Zurich earned them a shared 1939 Nobel Prize in Chemistry. Testosterone, now synthesizable in almost unlimited quantities, was identified as 17beta-hydroxandrost-4-en-3-one (C19H28O2), a solid polycyclic alcohol with a hydroxyl group at the 17th carbon atom. The presence of the hydroxyl group proved important, for two reasons.
First, the hydroxyl group made it obvious that testosterone could be esterified, or altered by the substitution of an acid group for the hydroxyl group at the C17 position. Esterification lowers the water solubility of the molecule and increases its lipid solubility, permitting a sterile oil-based injectible to form a “depot” in the muscle, from which it is gradually released. Esterification temporarily deactivates the steroid molecule, because the presence of the large acid chain prevents the steroid from binding to androgen receptor (AR) molecules within muscle cells that promote protein synthesis. But, as the esterified steroid is gradually leached from the oily depot into the blood, esterases (acid-cleaving molecules) replace the acid chain with a hydroxyl group as in the virgin molecule, permitting the steroid to bind to AR. The overall effect of esterification is to extend the steroid’s half-life, ease its administration, and alter its anabolic/androgenic ratio (A/AR), or the degree to which it affects striated muscle vs. sexual organ tissues such as the testes or prostate.
The partial synthesis in the 1930’s of abundant, potent testosterone esters permitted the characterization of the hormone’s effects, so that Kochakian and Murlin (1936) were able to show that testosterone raised nitrogen retention (a mechanism central to anabolism) in the dog, after which Charles Kenyon’s group (Kenyon et al, 1940) was able to demonstrate both anabolic and androgenic effects of testosterone propionate in eunuchoidal men, boys, and women. The period of the early 1930’s to the 1950’s has been called “The Golden Age of Steroid Chemistry” (Schwarz, Onken & Schubert, 1999), and work during this period progressed quickly.
The second important implication of the hydroxyl side chain at the C-17 position was that it permitted, not just esterification, but also alkylation of the steroid molecule (substitution of an ethyl or methyl group for the hydroxyl group). Alkylation was to permit the development of oral steroids, the so-called “17-aa” or alkylated family of androgens such as methyltestosterone, which could be taken up by the digestive track, and so be easily administered in pill form. Research in The Golden Age of Steroid Chemistry proved that this newly synthesized compound – testosterone – or rather family of compounds (for many derivatives were developed in the 1940’s, 50’s and 60’s), was a potent multiplier of muscle, strength, and wellbeing (deKruif, 1945).
A 2001 study[2] examined the effect of a 3-week period of sexual abstinence followed by masturbation-induced orgasm. It found that abstinence over such periods "does not change the neuroendocrine response to orgasm but does produce elevated levels of testosterone in males."
A 2003 study showed that serum testosterone levels reach a peak seven days after abstaining from ejaculation.