Testosterone is the primary male sex hormone and anabolic steroid. In male humans, testosterone plays a key role in the development of male reproductive tissues such as testes and prostates, as well as promotes secondary sexual characteristics such as increased muscle and bone mass, and body hair growth. In addition, testosterone is involved in health and well-being, and prevention of osteoporosis. Insufficient testosterone levels in men can cause abnormalities including frailty and bone loss.
Testosterone is a steroid of the androstane class containing keto and hydroxyl groups at three and seventeen positions each. It is synthesized in a few steps of cholesterol and converted in the liver into an inactive metabolite. This provides its action through the binding and activation of androgen receptors. In humans and most other vertebrates, testosterone is secreted mainly by male testes and, to a lesser extent, female ovaries. On average, in adult men, testosterone levels are about 7 to 8 times greater than in adult women. Because the metabolism of testosterone in males is greater, daily production is about 20 times greater in males. Women are also more sensitive to hormones.
In addition to its role as a natural hormone, testosterone is used as a drug, for example in the treatment of low testosterone levels in men and breast cancer in women. Because testosterone levels decline with age, testosterone is sometimes used in older men to overcome this deficiency. It is also used unlawfully to improve physical and performance, for example athletes. For more information on testosterone as a drug, see the article testosterone (drug).
Video Testosterone
Biological effects
In general, androgens such as testosterone increase protein synthesis and tissue growth with androgen receptors. Testosterone can be described as having virilising and anabolic effects (although this categorical description is somewhat arbitrary, since there is a lot of overlap between them).
- Anabolic effects include growth in muscle mass and strength, increased bone density and strength, and stimulation of linear growth and bone maturation. Androgenic effects include the maturation of sex organs, particularly penis and scrotum formation in the fetus, and after birth (usually at puberty) deepening of voice, facial hair growth (Like beard) and armpit hair (armpits). Many of these belong to the category of male secondary sex characteristics.
The effects of testosterone can also be classified by the age of the usual occurrence. For postnatal effects in both men and women, this largely depends on the level and duration of circulating free testosterone.
Before birth
Preoperative effects are divided into two categories, classified in relation to the stage of development.
The first period occurs between 4 and 6 weeks of pregnancy. Examples include genital virilization such as midline fusion, falus urethra, thinning and scrotum enlargement, and phalic enlargement; although the role of testosterone is much smaller than that of dihydrotestosterone. There is also the development of prostate gland and seminal vesicles.
During the second trimester, androgen levels are associated with gender formation. This period affects the femininization or masculinisation of the fetus and can be a better predictor of feminine or masculine behavior such as sex behavior typed from the adult level alone. Maternal testosterone levels during pregnancy correlate with girls' sex behavior as adults, and their correlations are even stronger than with their own adult testosterone levels.
early age
The baby's early androgen effects are the least understood. In the first weeks of the baby boy's life, testosterone levels rise. The levels remain within the puberty range for several months, but usually reach an almost undetectable level in childhood by 4-6 months of age. The function of this increase in humans is unknown. It has been theorized that brain masculinisation occurs because no significant changes have been identified in other parts of the body. The male brain is masculinized by the aromatization of testosterone into estrogen, which crosses the blood-brain barrier and enters the male brain, whereas the female fetus has -fetoprotein, which binds the estrogen so that the female brain is not affected.
Before puberty
Before puberty, the effects of androgen levels increase occur in boys and girls. These include adult body odor, increased oily properties of the skin and hair, acne, pubarche, axillary hair, accelerated growth, accelerated bone maturation, and facial hair.
Pubertal
The effects of puberty begin to occur when androgens have been higher than normal adult female levels for months or years. In men, this is a delayed public puberty effect, and occurs in women after a period of elevated levels of prolonged free testosterone in the blood. The effects include:
The growth of spermatogenic tissue in the testes, male fertility, penis enlargement or clitoris, increased libido and the frequency of erection or swelling of the clitoris. Growth of the jaw, eyebrow, chin, nose, and remodeling of facial bone contour, in conjunction with human growth hormone. Improved bone maturation and cessation of growth. This occurs indirectly through estradiol metabolites and therefore more gradually in men than women. Increased muscle and mass strength, shoulder becomes wider and ribs expands, deepening sounds, growth of Adam's apple. Enlarged sebaceous glands. This can cause acne, subcutaneous fat in the face decreases. The pubic hair extends to the thigh and towards the umbilicus, the development of facial hair (sideburns, beard, mustache), hair loss (androgenetic alopecia), increased chest hair, periareolar hair, perianal hair, leg hair, armpit hair.
Adult
Testosterone is required for normal sperm development. It activates genes in Sertoli cells, which promote differentiation of spermatogonia. This regulates the acute HPA response (hypothalamic-pituitary-adrenal axis) under the challenge of dominance. Androgens including testosterone promote muscle growth. Testosterone also regulates the population of thromboxane receptors A 2 on megakaryocytes and platelets and therefore platelet aggregation in humans.
The effects of adult testosterone are more clearly seen in males than females, but are likely to be important for both sexes. Some of these effects may decrease as testosterone levels may decline in the next decade of adult life.
Health risks
Testosterone does not appear to increase the risk of developing prostate cancer. In people who have undergone testosterone deprivation therapy, increased testosterone beyond castration levels has been shown to increase the extent of spread of existing prostate cancer.
Conflicting results have been obtained regarding the importance of testosterone in maintaining cardiovascular health. However, maintaining normal testosterone levels in elderly men has been shown to increase many parameters that are thought to reduce the risk of cardiovascular disease, such as an increase in lean body mass, decreased visceral fat mass, total cholesterol reduction, and glycemic control.
High androgen levels are associated with irregularity of the menstrual cycle in both clinical populations and healthy women.
Sexual stimulation
When testosterone and endorphins in cement ejaculation meet the cervical wall after intercourse, women receive testosterone, endorphin, and oxytocin spikes, and men after orgasm during copulation have increased endorphins and marked elevations in oxytocin levels. This adds to the friendly physiological environment in the woman's internal reproductive tract to conceive, and then to nurture the concept in the pre-embryonic stage, and to stimulate the feelings of love, desire, and care of the father in men (this is the only time male level oxytocin rivals women.
The level of testosterone follows a nyctohemeral rhythm that peaks earlier every day, regardless of sexual activity.
There is a positive correlation between the experience of positive orgasm in women and testosterone levels where relaxation is a key perception of experience. There is no correlation between testosterone and male perception of their orgasmic experiences, nor is there a correlation between higher testosterone levels and greater sexual assertiveness in both sexes.
Sexual impulse and masturbation in women result in small increases in testosterone concentrations. Plasma levels of various steroids increased significantly after masturbation in men and testosterone levels correlated with these levels.
Mammalian studies
Studies conducted on mice showed that their sexual arousal levels are sensitive to testosterone decline. When testosterone-treated mice were given moderate levels of testosterone, their sexual behavior (copulation, partner preference, etc.) was continued, but not when given a low amount of the same hormone. Therefore, these mammals can provide models for studying clinical populations among men who suffer from sexual arousal deficits such as hypoactive sexual desire disorders.
In every species of mammals examined showed a marked increase in male testosterone levels when meeting a woman novel . Increased reflexive testosterone in male mice is associated with early levels of male sexual arousal.
In non-human primates, perhaps testosterone in puberty stimulates sexual arousal, allowing primates to increasingly seek sexual experiences with women and thereby create a sexual preference for women. Some studies have also shown that if testosterone is removed in adult male or other adult male primate systems, the sexual motivation decreases, but there is no corresponding decrease in the ability to engage in sexual activity (installation, ejaculation, etc.).
The theory of sperm competition: Testosterone levels have been shown to increase in response to previous neutral stimuli when conditioned to become sexual in male rats. This reaction involves penile reflexes (such as erection and ejaculation) that aid in sperm competition when more than one male is present in an arranged marriage, allowing for successful sperm production and higher reproductive opportunities.
Men
In men, higher testosterone levels are associated with periods of sexual activity. Testosterone is also elevated in heterosexual men after having a brief conversation with a woman. An increase in testosterone levels is associated with a level that women think men try to impress them.
Men who watched sexually explicit films had an average increase of 35% in testosterone, peaking at 60-90 minutes after the end of the film, but no increase was seen in men who watched sexually neutral films. Men who watched sexually explicit films also reported increased motivation, competitiveness, and fatigue decline. A relationship has also been found between relaxation after sexual arousal and testosterone levels.
Male testosterone levels, a hormone known to affect male marital behavior, change depending on whether they are exposed to ovulating or ovulating women's bodies. Men exposed to the scent of ovulatory women maintain a stable level of testosterone higher than testosterone levels in men exposed to nonovulated signaling. Testosterone levels and sexual arousal in men are well aware of the hormonal cycle in women. This may be related to the hypodesis of ovulation shifts , in which males are adapted to respond to the ovulation cycle of women by sensing when they are most fertile and where women seek the preferred male partner when they are the most fertile; both actions may be driven by hormones.
Men with lower bounds for sexual arousal are more likely to attend sexual and testosterone information that can work by raising their attention to relevant stimuli.
Female
Androgens can modulate the physiology of the vaginal tissues and contribute to female genital sexual arousal. Women's testosterone levels are higher when measured pre-intercourse vs pre-hugging, as well as post-intercourse vs post-hugging. There is a time lag effect when testosterone is given, in the genital arousal in women. In addition, a persistent increase in vaginal sexual desire can lead to higher genital sensations and sexual behavior.
When women have higher testosterone levels, they have a higher increase in sexual arousal levels but a smaller increase in testosterone, suggesting a ceiling effect on testosterone levels in women. Sexual thoughts also alter the level of testosterone but not the level of cortisol in a woman's body, and hormonal contraceptives may affect the variation in testosterone response to the sexual mind.
Testosterone may prove to be an effective treatment in female sexual arousal disorder, and is available as a dermal patch. No FDA-approved androgen preparations for the treatment of androgen insufficiency; However, it has been used off-label to treat low libido and sexual dysfunction in older women. Testosterone can be a treatment for postmenopausal women as long as they are effectively estrogen-treated.
Romantic relationship
Falling in love reduces male testosterone levels while increasing female testosterone levels. There has been speculation that changes in testosterone result in temporary reductions in behavioral differences between the sexes. However, it is recommended that once the "honeymoon phase" ends - about four years into a relationship - changes in testosterone levels are no longer clear. Men who produce less testosterone are more likely to be in a relationship and/or married, and men who produce more testosterone are more likely to divorce; However, causality can not be determined in this correlation. Marriage or commitment can lead to decreased testosterone levels. Single men who do not have relationship experience have lower testosterone levels than single men with experience. It is recommended that this single man with prior experience be in a more competitive state than their inexperienced counterparts. Married men who engage in bonding maintenance activities such as spending a day with their partner/and/or their child do not have different testosterone levels compared to the time when they were not involved in the activity. Collectively, these results suggest that the presence of competitive activity rather than bond maintenance activities is more relevant to changes in testosterone levels.
Men who produce more testosterone are more likely to have sex out of wedlock. Testosterone levels do not depend on the physical presence of the partner; male testosterone levels involved in urban and long distance relationship are the same. Physical presence may be necessary for women who are in a relationship for partner-testosterone interactions, in which the same partner city women have lower testosterone levels than women who have partnered long distances.
Fatherhood
The role of the father also lowers testosterone levels in men, suggesting that emotional changes and behaviors that occur encourage the care of the father. How testosterone levels change when a child is in trouble showing a father style. If the level decreases, then more empathy from the father than the father whose level rises.
Motivation
Testosterone levels play a major role in risk taking during financial decisions. Even in intellectual activities such as a chess tournament or a final exam, previous testosterone levels can accurately predict which individuals will be motivated to do their best.
Aggression and criminality
Most studies support the relationship between adult criminality and testosterone, although the relationship is simple if examined separately for each sex. Almost all juvenile delinquency and testosterone studies are not significant. Most studies have also found that testosterone is associated with behavior or personality traits related to criminality such as antisocial behavior and alcoholism. Much research has also been done on the relationship between the more common aggressive behavior/feelings and testosterone. About half the research has found a relationship and about half there is no relationship.
Testosterone is just one of many factors affecting aggression and the effects of previous experience and environmental stimuli have been found to be strongly correlated. Several studies have shown that testosterone derivatives estradiol (one form of estrogen) may play an important role in male aggression. The study also found that testosterone facilitates aggression by modulating vasopressin receptors in the hypothalamus.
Sex hormones can encourage fair behavior. For research subjects take part in behavioral experiments in which the distribution of some real money is decided. The rules allow both fair and unfair deals. The negotiating partner may then accept or reject the offer. The more fair the offer is, the less likely it is to be rejected by the negotiating partner. If no agreement is reached, no party gets anything. Test subjects with artificially enhanced levels of testosterone are generally made better, offerings are fairer than those receiving placebo, thereby reducing the risk of rejection of their bid to a minimum. Two later studies empirically confirmed these results. However men with high testosterone were significantly 27% less generous in the ultimatum game while men with the lowest testosterone were 560% more generous. The Annual NY Academy of Science has also found the use of anabolic steroids that increase testosterone is higher in adolescents, and this is associated with increased violence. The study also found provision of testosterone to increase verbal aggression and anger in some participants.
Testosterone is significantly correlated with aggression and competitive behavior and is directly facilitated by the latter. There are two theories about the role of testosterone in aggression and competition. The first is a challenging hypothesis that states that testosterone will increase during puberty thus facilitating reproductive and competitive behavior that will include aggression. Hence the challenge of competition among men of the species that facilitates aggression and violence. Studies have found a direct correlation between testosterone and dominance, especially among the most violent criminals in prisons who have the highest testosterone levels. The same study also found that fathers (those outside the competitive environment) had the lowest testosterone levels compared with other men.
The second theory is similar and is known as "the theory of neuroandrogenic evolution (ENA) about male aggression". Testosterone and other androgens have evolved to make masculinisation of the brain to be competitive even to harm the person and others. Thus, individuals with masculinized brains as a result of pre-natal and testosterone adult life and androgens increase their resource capability to survive, attract and copulate as many couples as possible. Brain masculinization is not only mediated by testosterone levels in the adult stage, but also exposure to testosterone in the womb as a fetus. Higher pre-natal testosterone is indicated by a low rate ratio as well as adult testosterone levels increase the risk of offense or aggression among male players in a soccer game. The study also found higher pre-natal testosterone or a lower digit ratio to correlate with higher aggression in men.
An increase in testosterone levels during a competition predicts aggression in men but not in women. Subjects who interacted with hand guns and experimental games showed increased testosterone and aggression. Natural selection may have developed men to be more sensitive to competitive challenges situations and the status and role of interaction of testosterone is an essential ingredient for aggressive behavior in this situation. Testosterone produces aggression by activating the subcortical area of ​​the brain, which can also be inhibited or suppressed by social norms or family situations while still manifesting in various intensities and ways through thoughts, anger, verbal aggression, competition, domination and physical violence. Testosterone mediates interest in cruel and abusive gestures in men by promoting a broader view of violent stimuli. Characteristics of the structural brain of specific testosterone can predict aggressive behavior in individuals.
Estradiol is known to correlate with aggression in male rats. In addition, the conversion of testosterone into estradiol regulates male aggression in the cheeks during the breeding season. Mice given anabolic steroids that increase testosterone are also more aggressively physical to provoke as a result of "threat sensitivity".
Brain
The brain is also affected by this sexual differentiation; the aromatase enzyme converts testosterone into estradiol responsible for masculinization of the brain in male rats. In humans, fetal brain masculinisation arises, by observation of gender preferences in patients with congenital androgen-forming disease or androgen-receptor function, to be associated with functional androgen receptors.
There are some differences between the male and female brains (probably the result of different levels of testosterone), one of which is the size: the male brain, on average, is larger. Men were found to have a total myelinated fiber length of 176,000 km at age 20, whereas in women the total length was 149,000 km (about 15% less).
No short-term effects on mood or behavior were found from 10 weeks of supraphysiologic testosterone dose in 43 healthy men. The correlation between testosterone and risk tolerance in career choice exists among women.
Attention, memory, and spatial ability are the main cognitive functions influenced by human testosterone. Preliminary evidence suggests that low testosterone levels may be a risk factor for cognitive decline and possibly for Alzheimer type dementia, a key argument in the treatment of life extension for the use of testosterone in anti-aging therapy. Much of the literature, however, shows a curved or even quadratic relationship between spatial performance and circulating testosterone, in which hypo and hypersecretion (less and excessive secretion) of circulating androgens have a negative effect on cognition.
Maps Testosterone
Biological activity
Steroid hormone activity
The effects of testosterone on humans and other vertebrates occur through multiple mechanisms: by activation of androgen receptors (directly or as DHT), and by conversion to estradiol and the activation of certain estrogen receptors. Androgens such as testosterone have also been found to bind and activate membrane androgen receptors.
Free testosterone (T) is transported into the cytoplasm of target tissue cells, where it can bind to the androgen receptor, or it can be reduced to 5? -dihidrotestosterone (DHT) by cytoplasmic enzyme 5? -reductase. DHT binds to the same androgen receptor even stronger than testosterone, so its androgenic potential is about 5 times that of T. The T receptor or DHT receptor complex undergoes a structural change that allows it to move to the cell nucleus and binds directly to the specific nucleotide sequence of the chromosomal DNA. The binding area is called the hormonal response element (HRE), and affects the transcription activity of certain genes, producing androgenic effects.
Androgen receptors occur in many different body tissue systems of vertebrates, and both men and women respond equally to the same level. Extremely different amounts of testosterone at prenatal, during puberty, and throughout life are part of the biological differences between men and women.
Bone and brain are two important tissues in humans where the main effect of testosterone is by aromatization on estradiol. In bone, estradiol accelerates hardening of the cartilage to the bone, leading to closure of epiphyses and growth conclusions. In the central nervous system, testosterone is aromatized to estradiol. Estradiol rather than testosterone serves as the most important feedback signal for the hypothalamus (mainly affecting LH secretion). In many mammals, the pre-perinatal or perinatal masculinization of the brain area is sexually dimorphic by estradiol derived from the testosterone program and then male sexual behavior.
Neurosteroid activity
Testosterone, through its active metabolite 3? -androstanediol, is a strong positive allosteric modulator of GABA receptors A .
Testosterone has been found to act as an antagonist of TrkA and p75 NTR , a receptor for nerve growth factor neurotrophin (NGF), with a high affinity (about 5 m). In contrast to testosterone, DHEA and DHEA sulfate have been found to act as the high affinity agonists of these receptors.
Testosterone is a sigma receptor antagonist? 1 (K i = 1.014 or 201Ã, nM). However, the testosterone concentration required to bind to receptors is well above even the total concentration of testosterone circulation in adult men (which range between 10 and 35m).
Biochemistry
Biosynthesis
Like other steroid hormones, testosterone comes from cholesterol (see figure). The first step in biosynthesis involves cholesterol-side cholesterol cleavage by cholesterol side cleavage enzymes (P450scc, CYP11A1), a cytochondrial cytochrome P450 oxidase with the loss of six carbon atoms to produce pregnenolone. In the next step, two additional carbon atoms are removed by CYP17A1 (17 "-hydroxylase/17,20-lyase) enzyme in the endoplasmic reticulum to produce various C 19 steroids. In addition, the 3-hydroxyl group is oxidized by 3? -hydroxyeroid dehydrogenase to produce androstenedione. In the final step and rate limitation, the C17 androstenedione ketone group is reduced by 17-hydroxisteroid dehydrogenase to produce testosterone.
The greatest amount of testosterone (& 95%) is produced by the testes in men, whereas the adrenal glands constitute most of the rest. Testosterone is also synthesized in a much smaller total amount in women by the adrenal glands, thecal cells from the ovaries, and, during pregnancy, by the placenta. In the testes, testosterone is produced by Leydig cells. 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 is transported bound to a specific plasma protein, sex hormone binding globulin (SHBG).
Rule
In men, testosterone is synthesized mainly in Leydig cells. The number of Leydig cells is in turn regulated by luteinizing hormone (LH) and follicle-stimulating hormone (FSH). In addition, the amount of testosterone produced by Leydig cells is under the control of LH, which regulates the expression of 17-hydroxisteroid dehydrogenase.
The amount of testosterone synthesized is governed by the hypothalamus-pituitary-testis axis (see figure on the right). When low testosterone levels, gonadotropin-releasing hormone (GnRH) is released by the hypothalamus, which in turn stimulates the pituitary gland to release FSH and LH. These last two hormones stimulate the testes to synthesize testosterone. Finally, elevated testosterone levels through negative feedback act on the hypothalamus and pituitary to inhibit the release of GnRH and FSH/LH, respectively.
Factors that affect testosterone levels may include:
- Age: The level of testosterone gradually decreases as a man ages. This effect is sometimes referred to as andropause or slow-onset hypogonadism.
- Exercise: Resistance training increases testosterone levels, but in older men, the increase can be avoided by protein consumption. Endurance training in men can lead to lower testosterone levels.
- Nutrients: Vitamin A deficiency can lead to less than optimal plasma testosterone levels. Secosteroid of vitamin D in the level of 400-1000 IU/d (10-25 Âμg/d) increases testosterone levels. Zinc deficiency lowers testosterone levels but excessive supplementation has no effect on serum testosterone.
- Weight loss: Weight loss can lead to increased testosterone levels. The fat cells synthesize the aromatase enzyme, which converts testosterone, the male sex hormone, into estradiol, the female sex hormone. However, there was no clear association between body mass index and testosterone levels found.
- Miscellaneous: Sleep : (REM sleep) raises the level of nocturnal testosterone. Behavior : Domination challenges can, in some cases, stimulate increased testosterone release in men. Medicines : Natural or man-made antigens including spearmint tea reduce testosterone levels. Licorice can decrease testosterone production and this effect is greater in women.
Distribution
The plasma proteins that bind testosterone are 98.0 to 98.5%, with 1.5 to 2.0% free or unbound. This is tied 65% on sex hormone binding globulin (SHBG) and 33% is weak in albumin.
Metabolism
Both testosterone and 5? -DHT is metabolized primarily in the liver. About 50% of testosterone is metabolized through conjugation into glucuronide testosterone and to a lesser extent testosterone sulfate by glucuronosyltransferases and sulfotransferases, respectively. An additional 40% of testosterone is metabolized in equal proportions to 17-ketosteroids androsterone and etiocholanolone through a combined action of 5? - and 5? -reductase, 3-hydroxisteroid dehydrogenase, and 17? -HSD, in that order. Androsterone and etiocholanolone are then in glucuronidated and at lower levels of sulfate equal to testosterone. The conjugated testosterone and its hepatic metabolites are released from the liver to the circulation and excreted in urine and bile. Only a small part (2%) of testosterone is excreted unchanged in urine.
In the 17-ketosteroid pathway of testosterone metabolism, testosterone is changed in the liver by 5? -reductase and 5? -reductase to 5? -DHT and inactive 5? -DHT, respectively. Then, 5? -DHT and 5? -DHT changed by 3? -HSD becomes 3 ?, 5? -androstanediol and 3 ?, 5? -androstanediol, respectively. Next, 3?, 5? -androstanediol and 3 ?, 5? -androstanediol changed by 17? -HSD becomes androsterone and etiocholanolone, followed by their conjugation and excretion. 3 ?, 5? -Androstanediol and 3 ?, 5? -androstanediol can also be formed in this path when 5? -DHT and 5? -DHT followed by 3? -HSD is not 3? -HSD, respectively, and they can then be converted into epiandrosterone and epietiocholanolone, respectively. A small portion of about 3% of testosterone is reversibly converted in liver into androstenedione by 17? -HSD.
In addition to conjugate and 17-ketosteroid pathways, testosterone can also be hydroxylated and oxidized in the liver by the P450 cytochrome enzyme, including CYP3A4, CYP3A5, CYP2C9, CYP2C19, and CYP2D6. 6? -Hydroxylation and at a lower level 16? -hydroxylation is the main transformation. 6? -hydroxylated testosterone is catalyzed mainly by CYP3A4 and to a lesser extent CYP3A5 and is responsible for 75 to 80% of metastolic P450-mediated testosterone metabolism. Besides 6? - and 16? -hydroxytestosterone, 1? -, 2?/? -, 11? -, and 15? -hydroxytestosterone also forms as a minor metabolite. Certain py50chy cytochrome enzymes such as CYP2C9 and CYP2C19 can also oxidize testosterone at position C17 to form androstenedione.
Two direct metabolites of testosterone, 5? -DHT and estradiol, are biologically important and can be established both in the liver and in the extrahepatic tissue. About 5 to 7% testosterone is converted by 5? -reductase to 5? -DHT, with circulation rate 5? -DHT is about 10% of testosterone, and about 0.3% testosterone is converted to estradiol by aromatase. 5? -Reductase is highly expressed in male reproductive organs (including prostate gland, seminal vesicle, and epididymid), skin, hair follicles, and brain and aromatase are highly expressed in adipose, bone and brain tissue. As many as 90% testosterone is changed to 5? -DHT in so-called androgenic networks with high 5-epoxy expression, and since the potential is several times greater than 5? -DHT as an AR agonist relative to testosterone, It is estimated that the effect of testosterone has a 2 to 3 fold potential in the tissue.
Level
Total testosterone levels in the body are 264-916 ng/dL in men aged 19 to 39 years, while the average testosterone level in adult men has been reported as 630 ng/dL. Testosterone levels in men decrease with age. In women, mean total testosterone levels have been reported 32.6 ng/dL. In women with hyperandrogenism, mean total testosterone levels have been reported to be 62.1 ng/dL.
Medical use
Testosterone is used as a drug for the treatment of men with too little or no natural testosterone production, certain forms of breast cancer, and gender dysphoria in transgender men. This is known as hormone replacement therapy (HRT) or testosterone replacement therapy (TRT), which maintains serum testosterone levels within the normal range. Decreased production of testosterone with age has led to interest in androgen replacement therapy. It is unclear whether the use of testosterone for low levels because of useful or harmful aging.
Testosterone is included in the list of essential medicines of the World Health Organization, which is the most important drug needed in basic healthcare systems. It is available as a generic drug. The price depends on the form of testosterone used. This can be given as a cream or transdermal patch applied to the skin, by injection to the muscle, as a tablet placed on the cheek, or by consumption.
Common side effects of testosterone drugs include acne, swelling, and breast enlargement in men. Serious side effects may include liver toxicity, heart disease, and behavioral changes. Exposed women and children can develop virilization. It is recommended that individuals with prostate cancer do not use drugs. May cause harm if used during pregnancy or lactation.
History
Testicular action associated with the circulation of blood fractions - now understood as the androgenic family of hormones - in the early work on castration and transplantation of testicles in poultry by Arnold Adolph Berthold (1803-1861). Research on the action of testosterone received a brief boost in 1889, when Harvard professor Charles-ÃÆ' â € ° douard Brown-SÃÆ' Â © quard (1817-1894), then in Paris, injected subcutaneously with a "rejuvenating potion" consisting of extracts dog testicles and guinea pigs. He reported in The Lancet that his strength and feelings were well restored but the effect was temporary, and Brown-SÃÆ' Â © quard's hopes for the complex were vanquished. Suffering derision from his colleagues, he abandoned his work on the mechanisms and effects of androgens in humans.
In 1927, University of Chicago Chemical Physiologist Fred C. Koch established easy access to a large source of Chicago bovin - stockyards testis and recruited students willing to bear the tedious work of extracting their isolates. That year, Koch and his pupil, Lemuel McGee, obtained 20 mg of substance from a supply of 40 pounds of testes bovin which, when administered to castrated cocks, pigs and rats, remasculinized them. The Ernst Laqueur group at the University of Amsterdam purified testosterone from bovine testis in the same way in 1934, but the isolation of hormones from animal tissues in the amount that allowed serious study in humans was not feasible until three European pharmaceutical giants - Schering (Berlin), Germany) Organon (Oss, The Netherlands) and Ciba (Basel, Switzerland) - began research and development of a full-scale steroid program in the 1930s.
Organon groups in the Netherlands were the first to isolate the hormone, identified in a May 1935 paper "On Crystalline Male Hormone from Testicles (Testosterone)". They named the testosterone hormone, from the stem of testicular and sterol, and the ketone suffix. The structure was done by Schering's Adolf Butenandt, at the Chemisches Institute from the Technical University at Gda? Sk.
Chemical synthesis of testosterone from cholesterol was achieved in August of that year by Butenandt and Hanisch. Only a week later, the Ciba group in Zurich, Leopold Ruzicka (1887-1976) and A. Wettstein, published their testosterone synthesis. This partial synthesis of independent testosterone from the cholesterol base received both Butenandt and Ruzicka along with the 1939 Nobel Prize in Chemistry. Testosterone identified as 17? -hydroxyandrost-4-en-3-one (C 19 H 28 2 ), solid polycyclic alcohols with hydroxyl groups on carbon atoms 17. It also makes clear that additional modifications to the synthesized testosterone can be performed, ie, esterification and alkylation.
Partial synthesis in the abundant 1930s, strong testosterone esters allows characterization of hormonal effects, so Kochakian and Murlin (1936) were able to show that testosterone increased the nitrogen retention (central mechanism for anabolism) in dogs, after which the Allan Kenyon group was able to show the effect anabolic and androgenic of testosterone propionate in men, women and eunuchoidal women. The period from the early 1930s to the 1950s has been called the "Golden Age of Chemical Steroids", and worked during this period rapidly. Research in this golden age proves that the newly synthesized compound - testosterone - or rather the family of compounds (for many derivatives developed from 1940 to 1960), is a powerful multiplier of strength, strength, and well-being.
Other animals
Testosterone is observed in most vertebrates. Testosterone and classical nuclear androgen receptors first appear in gnathostomes (jawed vertebrates). Agnathans (jawless vertebrates) such as lampreys do not produce testosterone but use androstenedione as male sex hormones. Fish make a slightly different shape called 11-ketotestosterone. The counter to the insect is ecdysone. The presence of steroids everywhere in various animals shows that sex hormones have an ancient evolutionary history.
See also
- List of androgen/anabolic steroids
References
Further reading
- Fargo KN, Pak TR, Foecking EM, Jones KJ (2010). "Molecular Biology Androgen Action: Perspective on Neuroprotective and Neurotherapeutic Effects.". At Pfaff DW, Etgen AM. The Molecular Mechanism of Hormone Actions on Behavior . Elsevier Inc. pp.Ã, 1219-1246. doi: 10.1016/B978-008088783-8.00036-X. ISBN 978-0-12-374939-0.
- Dowd, Nancy E. (2013). "Sperm, testosterone, masculinity and father". Nevada Law Journal, special edition: Men, Masculinity, and Law: A Symposium on Multidimensional Masculinity Theories . William S. Boyd School of Law. 13 (2): 8.
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