Stet

Testosterone - Wikipedia https://en.wikipedia.
org/wiki/Testosterone
Testosterone
Testosterone is the primary male sex hormone and an anabolic
Testosterone
steroid. In male humans, testosterone plays a key role in the
development of male reproductive tissues such as testes and
prostate, as well as promoting secondary sexual characteristics
such as increased muscle and bone mass, and the growth of body
hair.[3] In addition, testosterone is involved in health and well-
being,[4] and the prevention of osteoporosis.[5] Insufficient levels
of testosterone in men may lead to abnormalities including frailty
and bone loss.
Testosterone is a steroid from the androstane class containing a

keto and hydroxyl groups at the three and seventeen positions
respectively. It is biosynthesized in several steps from cholesterol
and is converted in the liver to inactive metabolites.[6] It exerts its
action through binding to and activation of the androgen
receptor.[6] In humans and most other vertebrates, testosterone is
secreted primarily by the testicles of males and, to a lesser extent,
Names
the ovaries of females. On average, in adult males, levels of
testosterone are about 7 to 8 times as great as in adult females.[7] IUPAC name
As the metabolism of testosterone in males is more pronounced, 17β-Hydroxyandrost-4-en-3-one
the daily production is about 20 times greater in men.[8][9] Systematic IUPAC name
Females are also more sensitive to the hormone.[10] (8R,9S,10R,13S,14S,17S)-17-Hydroxy-
10,13-dimethyl-
In addition to its role as a natural hormone, testosterone is used as 1,2,6,7,8,9,11,12,14,15,16,17-
a medication, for instance in the treatment of low testosterone dodecahydrocyclopenta[a]phenanthren-3-
one
levels in men, transgender hormone therapy for transgender men,
and breast cancer in women.[11] Since testosterone levels decrease Other names
as men age, testosterone is sometimes used in older men to Androst-4-en-17β-ol-3-one
counteract this deficiency. It is also used illicitly to enhance Identifiers
physique and performance, for instance in athletes. CAS Number 58-22-0 (http://www.comm
onchemistry.org/Chemical
Detail.aspx?ref=58-22-0)
Contents 3D model Interactive image (https://c
(JSmol) hemapps.stolaf.edu/jmol/j
Biological effects
Before birth mol.php?model=O%3DC
Early infancy 4%5CC%3DC2%2F%5B
Before puberty C%40%5D%28%5BC%40
Pubertal H%5D1CC%5BC%40%4
Adult 0%5D3%28%5BC%40%4
Aggression and criminality
0H%5D%28O%29CC%5B
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Testosterone - Wikipedia https://en.wikipedia.org/wiki/Testosterone
Brain C%40H%5D3%5BC%4
Immune system and inflammation 0%40H%5D1CC2%29C%
29%28C%29CC4)
Medical use
Biological activity ChEBI CHEBI:17347 (https://ww
Steroid hormone activity w.ebi.ac.uk/chebi/searchI
Neurosteroid activity d.do?chebiId=17347)
Biochemistry ChEMBL ChEMBL386630 (https://w
Biosynthesis
ww.ebi.ac.uk/chembldb/in
Distribution
Metabolism dex.php/compound/inspec
Levels t/ChEMBL386630)
Measurement ChemSpider 5791 (http://www.chemspi

History der.com/Chemical-Structu
Other animals re.5791.html)
See also DrugBank DB00624 (https://www.dru
References gbank.ca/drugs/DB00624)
Further reading
ECHA InfoCard 100.000.336 (https://echa.
europa.eu/substance-infor
Biological effects mation/-/substanceinfo/10
In general, androgens such as testosterone promote protein 0.000.336)
synthesis and thus growth of tissues with androgen receptors.[12] KEGG D00075 (https://www.keg
Testosterone can be described as having virilising and anabolic g.jp/entry/D00075)
effects (though these categorical descriptions are somewhat PubChem CID 6013 (https://pubchem.nc
arbitrary, as there is a great deal of mutual overlap between
bi.nlm.nih.gov/compound/
them).[13]
6013)
Anabolic effects include growth of muscle mass and strength, UNII 3XMK78S47O (https://fda
increased bone density and strength, and stimulation of linear
growth and bone maturation. sis.nlm.nih.gov/srs/srsdire
Androgenic effects include maturation of the sex organs, ct.jsp?regno=3XMK78S47
particularly the penis and the formation of the scrotum in the O)
fetus, and after birth (usually at puberty) a deepening of the
voice, growth of facial hair (such as the beard) and axillary CompTox DTXSID8022371 (https://c
(underarm) hair. Many of these fall into the category of male Dashboard omptox.epa.gov/dashboar
secondary sex characteristics. (EPA)
d/DTXSID8022371)
Testosterone effects can also be classified by the age of usual
occurrence. For postnatal effects in both males and females, these InChI
are mostly dependent on the levels and duration of circulating free SMILES
testosterone. Properties
Chemical C19H28O2
Before birth formula
Molar mass 288.431 g·mol−1
Effects before birth are divided into two categories, classified in
relation to the stages of development. Melting point 151.0 °C (303.8 °F;
424.1 K)[1]
The first period occurs between 4 and 6 weeks of the gestation.
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Examples include genital virilisation such as midline fusion, phallic Pharmacology

urethra, scrotal thinning and rugation, and phallic enlargement;
ATC code G03BA03 (WHO (https://w
although the role of testosterone is far smaller than that of
ww.whocc.no/atc_ddd_ind
dihydrotestosterone. There is also development of the prostate
ex/?code=G03BA03))
gland and seminal vesicles.
License data EU EMA: by INN (http://ww
During the second trimester, androgen level is associated with sex w.ema.europa.eu/ema/ind
formation.[14] Specifically, testosterone, along with anti-Müllerian ex.jsp?curl=%2Fpages%2
hormone (AMH) promote growth of the Wolffian duct and Fmedicines%2Flanding%
degeneration of the Müllerian duct respectively.[15] This period 2Fepar_search.jsp&mid=&
affects the femininization or masculinization of the fetus and can searchTab=searchByKey&
be a better predictor of feminine or masculine behaviours such as alreadyLoaded=true&isNe
sex typed behaviour than an adult's own levels. Prenatal androgens wQuery=true&status=Auth
apparently influence interests and engagement in gendered orised&status=Withdraw
activities and have moderate effects on spatial abilities.[16] Among n&status=Suspended&stat
women with CAH, a male-typical play in childhood correlated with us=Refused&keywordSea
reduced satisfaction with the female gender and reduced rch=Submit&searchType=i
heterosexual interest in adulthood.[17] nn&taxonomyPath=&tree
Number=&searchGeneric
Type=generics&keyword=
Early infancy Testosterone)
Early infancy androgen effects are the least understood. In the first Routes of Transdermal (gel, cream,
weeks of life for male infants, testosterone levels rise. The levels administration solution, patch), by mouth
remain in a pubertal range for a few months, but usually reach the (as testosterone
barely detectable levels of childhood by 4–7 months of age.[18][19] undecanoate), in the
The function of this rise in humans is unknown. It has been cheek, intranasal (gel),
theorized that brain masculinization is occurring since no intramuscular injection (as
significant changes have been identified in other parts of the esters), subcutaneous
body.[20] The male brain is masculinized by the aromatization of pellets
testosterone into estrogen, which crosses the blood–brain barrier
Pharmacokinetics:
and enters the male brain, whereas female fetuses have
Bioavailability Oral: very low (due to
α-fetoprotein, which binds the estrogen so that female brains are
extensive first pass
not affected.[21]
metabolism)
Protein binding 97.0–99.5% (to SHBG
Before puberty and albumin)[2]
Before puberty effects of rising androgen levels occur in both boys Metabolism Liver (mainly reduction
and girls. These include adult-type body odor, increased oiliness of and conjugation)
skin and hair, acne, pubarche (appearance of pubic hair), axillary
Biological half- 2–4 hours
hair (armpit hair), growth spurt, accelerated bone maturation, and life
facial hair.[22] Excretion Urine (90%), feces (6%)
Except where otherwise noted, data are
Pubertal given for materials in their standard state (at
25 °C [77 °F], 100 kPa).
Pubertal effects begin to occur when androgen has been higher
verify (what is ?)
than normal adult female levels for months or years. In males,
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these are usual late pubertal effects, and occur in women after Infobox references
prolonged periods of heightened levels of free testosterone in the
blood. The effects include:[22][23]
Growth of spermatogenic tissue in testicles, male fertility, penis or clitoris enlargement, increased libido and frequency
of erection or clitoral engorgement occurs. Growth of jaw, brow, chin, and nose and remodeling of facial bone contours,
in conjunction with human growth hormone occurs.[24] Completion of bone maturation and termination of growth.
This occurs indirectly via estradiol metabolites and hence more gradually in men than women. Increased muscle
strength and mass, shoulders become broader and rib cage expands, deepening of voice, growth of the Adam's apple.
Enlargement of sebaceous glands. This might cause acne, subcutaneous fat in face decreases. Pubic hair extends to
thighs and up toward umbilicus, development of facial hair (sideburns, beard, moustache), loss of scalp hair
(androgenetic alopecia), increase in chest hair, periareolar hair, perianal hair, leg hair, armpit hair.
Adult
Testosterone is necessary for normal sperm development. It activates genes in Sertoli cells, which promote
differentiation of spermatogonia. It regulates acute HPA (hypothalamic–pituitary–adrenal axis) response under
dominance challenge.[25] Androgen including testosterone enhances muscle growth. Testosterone also regulates the
population of thromboxane A2 receptors on megakaryocytes and platelets and hence platelet aggregation in humans.
[26][27]
Adult testosterone effects are more clearly demonstrable in males than in females, but are likely important to both
sexes. Some of these effects may decline as testosterone levels might decrease in the later decades of adult life.[28]
Health risks
Testosterone does not appear to increase the risk of developing prostate cancer. In people who have undergone
testosterone deprivation therapy, testosterone increases beyond the castrate level have been shown to increase the rate
of spread of an existing prostate cancer.[29][30][31]
Conflicting results have been obtained concerning the importance of testosterone in maintaining cardiovascular health.
[32][33] Nevertheless, maintaining normal testosterone levels in elderly men has been shown to improve many
parameters that are thought to reduce cardiovascular disease risk, such as increased lean body mass, decreased visceral
fat mass, decreased total cholesterol, and glycemic control.[34]
High androgen levels are associated with menstrual cycle irregularities in both clinical populations and healthy
women.[35]
Sexual arousal
When testosterone and endorphins in ejaculated semen meet the cervical wall after sexual intercourse, females receive a
spike in testosterone, endorphin, and oxytocin levels, and males after orgasm during copulation experience an increase
in endorphins and a marked increase in oxytocin levels. This adds to the hospitable physiological environment in the
female internal reproductive tract for conceiving, and later for nurturing the conceptus in the pre-embryonic stages, and
stimulates feelings of love, desire, and paternal care in the male (this is the only time male oxytocin levels rival a
female's).
Testosterone levels follow a nyctohemeral rhythm that peaks early each day, regardless of sexual activity.[36]
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There are positive correlations between positive orgasm experience in women and testosterone levels where relaxation
was a key perception of the experience. There is no correlation between testosterone and men's perceptions of their
orgasm experience, and also no correlation between higher testosterone levels and greater sexual assertiveness in either
sex.[37]
Sexual arousal and masturbation in women produce small increases in testosterone concentrations.[38] The plasma
levels of various steroids significantly increase after masturbation in men and the testosterone levels correlate to those
levels.[39]
Mammalian studies
Studies conducted in rats have indicated that their degree of sexual arousal is sensitive to reductions in testosterone.
When testosterone-deprived rats were given medium levels of testosterone, their sexual behaviors (copulation, partner
preference, etc.) resumed, but not when given low amounts of the same hormone. Therefore, these mammals may
provide a model for studying clinical populations among humans suffering from sexual arousal deficits such as
hypoactive sexual desire disorder.[40]
Every mammalian species examined demonstrated a marked increase in a male's testosterone level upon encountering
a novel female. The reflexive testosterone increases in male mice is related to the male's initial level of sexual
arousal.[41]
In non-human primates, it may be that testosterone in puberty stimulates sexual arousal, which allows the primate to
increasingly seek out sexual experiences with females and thus creates a sexual preference for females.[42] Some
research has also indicated that if testosterone is eliminated in an adult male human or other adult male primate's
system, its sexual motivation decreases, but there is no corresponding decrease in ability to engage in sexual activity
(mounting, ejaculating, etc.).[42]
In accordance with sperm competition theory, testosterone levels are shown to increase as a response to previously
neutral stimuli when conditioned to become sexual in male rats.[43] This reaction engages penile reflexes (such as
erection and ejaculation) that aid in sperm competition when more than one male is present in mating encounters,
allowing for more production of successful sperm and a higher chance of reproduction.
Males
In men, higher levels of testosterone are associated with periods of sexual activity.[44][45]
Men who watch a sexually explicit movie have an average increase of 35% in testosterone, peaking at 60–90 minutes
after the end of the film, but no increase is seen in men who watch sexually neutral films.[46] Men who watch sexually
explicit films also report increased motivation, competitiveness, and decreased exhaustion.[47] A link has also been
found between relaxation following sexual arousal and testosterone levels.[48]
Men's levels of testosterone, a hormone known to affect men's mating behaviour, changes depending on whether they
are exposed to an ovulating or nonovulating woman's body odour. Men who are exposed to scents of ovulating women
maintained a stable testosterone level that was higher than the testosterone level of men exposed to nonovulation cues.
Testosterone levels and sexual arousal in men are heavily aware of hormone cycles in females.[49] This may be linked to
the ovulatory shift hypothesis,[50] where males are adapted to respond to the ovulation cycles of females by sensing
when they are most fertile and whereby females look for preferred male mates when they are the most fertile; both
actions may be driven by hormones.
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Females
Androgens may modulate the physiology of vaginal tissue and contribute to female genital sexual arousal.[51] Women's
level of testosterone is higher when measured pre-intercourse vs pre-cuddling, as well as post-intercourse vs post-
cuddling.[52] There is a time lag effect when testosterone is administered, on genital arousal in women. In addition, a
continuous increase in vaginal sexual arousal may result in higher genital sensations and sexual appetitive
behaviors.[53]
When females have a higher baseline level of testosterone, they have higher increases in sexual arousal levels but
smaller increases in testosterone, indicating a ceiling effect on testosterone levels in females. Sexual thoughts also
change the level of testosterone but not level of cortisol in the female body, and hormonal contraceptives may affect the
variation in testosterone response to sexual thoughts.[54]
Testosterone may prove to be an effective treatment in female sexual arousal disorders,[55] and is available as a dermal
patch. There is no FDA approved androgen preparation for the treatment of androgen insufficiency; however, it has
been used as an off-label use to treat low libido and sexual dysfunction in older women. Testosterone may be a
treatment for postmenopausal women as long as they are effectively estrogenized.[55]
Romantic relationships
Falling in love decreases men's testosterone levels while increasing women's testosterone levels. There has been
speculation that these changes in testosterone result in the temporary reduction of differences in behavior between the
sexes.[56] However, it is suggested that after the "honeymoon phase" ends—about four years into a relationship—this
change in testosterone levels is no longer apparent.[56] Men who produce less testosterone are more likely to be in a
relationship[57] or married,[58] and men who produce more testosterone are more likely to divorce;[58] however,
causality cannot be determined in this correlation. Marriage or commitment could cause a decrease in testosterone
levels.[59]
Single men who have not had relationship experience have lower testosterone levels than single men with experience. It
is suggested that these single men with prior experience are in a more competitive state than their non-experienced
counterparts.[60] Married men who engage in bond-maintenance activities such as spending the day with their spouse
and/or child have no different testosterone levels compared to times when they do not engage in such activities.
Collectively, these results suggest that the presence of competitive activities rather than bond-maintenance activities are
more relevant to changes in testosterone levels.[61]
Men who produce more testosterone are more likely to engage in extramarital sex.[58] Testosterone levels do not rely on
physical presence of a partner; testosterone levels of men engaging in same-city and long-distance relationships are
similar.[57] Physical presence may be required for women who are in relationships for the testosterone–partner
interaction, where same-city partnered women have lower testosterone levels than long-distance partnered women.[62]
Fatherhood
Fatherhood decreases testosterone levels in men, suggesting that the emotions and behavior tied to decreased
testosterone promote paternal care. In humans and other species that utilize allomaternal care, paternal investment in
offspring is beneficial to said offspring's survival because it allows the parental dyad to raise multiple children
simultaneously. This increases the reproductive fitness of the parents, because their offspring are more likely to survive
and reproduce. Paternal care increases offspring survival due to increased access to higher quality food and reduced
physical and immunological threats.[63] This is particularly beneficial for humans since offspring are dependent on
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parents for extended periods of time and mothers have relatively short inter-birth intervals.[64]
While extent of paternal care varies between cultures, higher investment in direct child care has been seen to be
correlated with lower average testosterone levels as well as temporary fluctuations.[65] For instance, fluctuation in
testosterone levels when a child is in distress has been found to be indicative of fathering styles. If a father's testosterone
levels decrease in response to hearing their baby cry, it is an indication of empathizing with the baby. This is associated
with increased nurturing behavior and better outcomes for the infant.[66]
Motivation
Testosterone levels play a major role in risk-taking during financial decisions.[67][68]
Aggression and criminality

Most studies support a link between adult criminality and testosterone. Nearly all studies of juvenile delinquency and
testosterone are not significant. Most studies have also found testosterone to be associated with behaviors or
personality traits linked with criminality such as antisocial behavior and alcoholism. Many studies have also been done
on the relationship between more general aggressive behavior and feelings and testosterone. About half the studies have
found a relationship and about half no relationship.[69] Studies have also found that testosterone facilitates aggression
by modulating vasopressin receptors in the hypothalamus.[70]
Testosterone is significantly discussed in relation to aggression and competitive behavior. There are two theories on the
role of testosterone in aggression and competition.[71] The first one is the challenge hypothesis which states that
testosterone would increase during puberty, thus facilitating reproductive and competitive behavior which would
include aggression.[71] It is therefore the challenge of competition among males of the species that facilitates aggression
and violence.[71] Studies conducted have found direct correlation between testosterone and dominance, especially
among the most violent criminals in prison who had the highest testosterone levels.[71] The same research also found
fathers (those outside competitive environments) had the lowest testosterone levels compared to other males.[71]
The second theory is similar and is known as "evolutionary neuroandrogenic (ENA) theory of male aggression".[72][73]
Testosterone and other androgens have evolved to masculinize a brain in order to be competitive even to the point of
risking harm to the person and others. By doing so, individuals with masculinized brains as a result of pre-natal and
adult life testosterone and androgens enhance their resource acquiring abilities in order to survive, attract and copulate
with mates as much as possible.[72] The masculinization of the brain is not just mediated by testosterone levels at the
adult stage, but also testosterone exposure in the womb as a fetus. Higher pre-natal testosterone indicated by a low digit
ratio as well as adult testosterone levels increased risk of fouls or aggression among male players in a soccer game.[74]
Studies have also found higher pre-natal testosterone or lower digit ratio to be correlated with higher aggression in
males.[75][76][77][78][79]
The rise in testosterone levels during competition predicted aggression in males but not in females.[80] Subjects who
interacted with hand guns and an experimental game showed rise in testosterone and aggression.[81] Natural selection
might have evolved males to be more sensitive to competitive and status challenge situations and that the interacting
roles of testosterone are the essential ingredient for aggressive behaviour in these situations.[82] Testosterone produces
aggression by activating subcortical areas in the brain, which may also be inhibited or suppressed by social norms or
familial situations while still manifesting in diverse intensities and ways through thoughts, anger, verbal aggression,
competition, dominance and physical violence.[83] Testosterone mediates attraction to cruel and violent cues in men by
promoting extended viewing of violent stimuli.[84] Testosterone specific structural brain characteristic can predict
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aggressive behaviour in individuals.[85]
Testosterone might encourage fair behavior. For one study, subjects took part in a behavioral experiment where the
distribution of a real amount of money was decided. The rules allowed both fair and unfair offers. The negotiating
partner could subsequently accept or decline the offer. The fairer the offer, the less probable a refusal by the negotiating
partner. If no agreement was reached, neither party earned anything. Test subjects with an artificially enhanced
testosterone level generally made better, fairer offers than those who received placebos, thus reducing the risk of a
rejection of their offer to a minimum. Two later studies have empirically confirmed these results.[86][87][88] However
men with high testosterone were significantly 27% less generous in an ultimatum game.[89] The Annual NY Academy of
Sciences has also found anabolic steroid use (which increases testosterone) to be higher in teenagers, and this was
associated with increased violence.[90] Studies have also found administered testosterone to increase verbal aggression
and anger in some participants.[91]
A few studies indicate that the testosterone derivative estradiol (one form of estrogen) might play an important role in
male aggression.[69][92][93][94] Estradiol is known to correlate with aggression in male mice.[95] Moreover, the
conversion of testosterone to estradiol regulates male aggression in sparrows during breeding season.[96] Rats who were
given anabolic steroids that increase testosterone were also more physically aggressive to provocation as a result of
"threat sensitivity".[97]
Brain
The brain is also affected by this sexual differentiation;[14] the enzyme aromatase converts testosterone into estradiol
that is responsible for masculinization of the brain in male mice. In humans, masculinization of the fetal brain appears,
by observation of gender preference in patients with congenital diseases of androgen formation or androgen receptor
function, to be associated with functional androgen receptors.[98]
There are some differences between a male and female brain (possibly the result of different testosterone levels), one of
them being size: the male human brain is, on average, larger.[99] Men were found to have a total myelinated fiber length
of 176 000 km at the age of 20, whereas in women the total length was 149 000 km (approx. 15% less).[100]
No immediate short term effects on mood or behavior were found from the administration of supraphysiologic doses of
testosterone for 10 weeks on 43 healthy men.[101] A correlation between testosterone and risk tolerance in career choice
exists among women.[67][102]
Attention, memory, and spatial ability are key cognitive functions affected by testosterone in humans. Preliminary
evidence suggests that low testosterone levels may be a risk factor for cognitive decline and possibly for dementia of the
Alzheimer's type,[103][104][105][106] a key argument in life extension medicine for the use of testosterone in anti-aging
therapies. Much of the literature, however, suggests a curvilinear or even quadratic relationship between spatial
performance and circulating testosterone,[107] where both hypo- and hypersecretion (deficient- and excessive-secretion)
of circulating androgens have negative effects on cognition.
Immune system and inflammation

Testosteone deficiency is associated with an increased risk of metabolic syndrome, cardiovascular disease and mortality,
which are also sequelae of chronic inflammation.[108] Testosterone plasma concentration inversely correlates to
multiple biomarkers of inflammation including CRP, interleukin 1 beta, interleukin 6, TNF alpha and endotoxin
concentration, as well as leukocyte count.[108] As demonstrated by a meta-analysis, substitution therapy with
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testosterone results in a significant reduction of inflammatory markers.[108] These effects are mediated by different
mechanisms with synergistic action.[108] In androgen-deficient men with concomitant autoimmune thyroiditis,
substitution therapy with testosterone leads to a decrease in thyroid autoantibody titres and an increase in thyroid's
secretory capacity (SPINA-GT).[109]
Medical use
Testosterone is used as a medication for the treatment of males with too little or no natural testosterone production,
certain forms of breast cancer,[11] and gender dysphoria in transgender men. This is known as hormone replacement
therapy (HRT) or testosterone replacement therapy (TRT), which maintains serum testosterone levels in the normal
range. Decline of testosterone production with age has led to interest in androgen replacement therapy.[110] It is unclear
if the use of testosterone for low levels due to aging is beneficial or harmful.[111]
Testosterone is included in the World Health Organization's list of essential medicines, which are the most important
medications needed in a basic health system.[112] It is available as a generic medication.[11] The price depends on the
form of testosterone used.[113] It can be administered as a cream or transdermal patch that is applied to the skin, by
injection into a muscle, as a tablet that is placed in the cheek, or by ingestion.[11]
Common side effects from testosterone medication include acne, swelling, and breast enlargement in males.[11] Serious
side effects may include liver toxicity, heart disease, and behavioral changes.[11] Women and children who are exposed
may develop virilization.[11] It is recommended that individuals with prostate cancer not use the medication.[11] It can
cause harm if used during pregnancy or breastfeeding.[11]
Biological activity
Steroid hormone activity

The effects of testosterone in humans and other vertebrates occur by way of multiple mechanisms: by activation of the
androgen receptor (directly or as DHT), and by conversion to estradiol and activation of certain estrogen receptors.
[114][115] Androgens such as testosterone have also been found to bind to and activate membrane androgen receptors.
[116][117][118]
Free testosterone (T) is transported into the cytoplasm of target tissue cells, where it can bind to the androgen receptor,
or can be reduced to 5α-dihydrotestosterone (DHT) by the cytoplasmic enzyme 5α-reductase. DHT binds to the same
androgen receptor even more strongly than testosterone, so that its androgenic potency is about 5 times that of T.[119]
The T-receptor or DHT-receptor complex undergoes a structural change that allows it to move into the cell nucleus and
bind directly to specific nucleotide sequences of the chromosomal DNA. The areas of binding are called hormone
response elements (HREs), and influence transcriptional activity of certain genes, producing the androgen effects.
Androgen receptors occur in many different vertebrate body system tissues, and both males and females respond
similarly to similar levels. Greatly differing amounts of testosterone prenatally, at puberty, and throughout life account
for a share of biological differences between males and females.
The bones and the brain are two important tissues in humans where the primary effect of testosterone is by way of
aromatization to estradiol. In the bones, estradiol accelerates ossification of cartilage into bone, leading to closure of the
epiphyses and conclusion of growth. In the central nervous system, testosterone is aromatized to estradiol. Estradiol
rather than testosterone serves as the most important feedback signal to the hypothalamus (especially affecting LH
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secretion).[120] In many mammals, prenatal or perinatal "masculinization" of the sexually dimorphic areas of the brain
by estradiol derived from testosterone programs later male sexual behavior.[121]
Neurosteroid activity
Testosterone, via its active metabolite 3α-androstanediol, is a potent positive allosteric modulator of the GABAA
receptor.[122]
Testosterone has been found to act as an antagonist of the TrkA and p75NTR, receptors for the neurotrophin nerve
growth factor (NGF), with high affinity (around 5 nM).[123][124][125] In contrast to testosterone, DHEA and DHEA
sulfate have been found to act as high-affinity agonists of these receptors.[123][124][125]
Testosterone is an antagonist of the sigma σ1 receptor (Ki = 1,014 or 201 nM).[126] However, the concentrations of
testosterone required for binding the receptor are far above even total circulating concentrations of testosterone in adult
males (which range between 10 and 35 nM).[127]
Biochemistry
Biosynthesis
Like other steroid hormones,
testosterone is derived from
cholesterol (see figure).[129]
The first step in the
biosynthesis involves the
oxidative cleavage of the
side-chain of cholesterol by
cholesterol side-chain
cleavage enzyme (P450scc,
CYP11A1), a mitochondrial
cytochrome P450 oxidase
with the loss of six carbon
atoms to give pregnenolone.
In the next step, two
additional carbon atoms are
removed by the CYP17A1
(17α-hydroxylase/17,20-
lyase) enzyme in the
endoplasmic reticulum to
yield a variety of C19 Human steroidogenesis, showing testosterone near bottom.[128]
steroids.[130] In addition, the
3β-hydroxyl group is
oxidized by 3β-hydroxysteroid dehydrogenase to produce androstenedione. In the final and rate limiting step, the C17
keto group androstenedione is reduced by 17β-hydroxysteroid dehydrogenase to yield testosterone.
The largest amounts of testosterone (>95%) are produced by the testes in men,[3] while the adrenal glands account for
10 of 34 28/11/2019, 23:49
most of the remainder. Testosterone is also synthesized in far smaller total quantities in women by the adrenal glands,
thecal cells of the ovaries, and, during pregnancy, by the placenta.[131] In the testes, testosterone is produced by the
Leydig cells.[132] 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).
Regulation
In males, testosterone is synthesized primarily in Leydig cells. The number
of Leydig cells in turn is regulated by luteinizing hormone (LH) and follicle-
stimulating hormone (FSH). In addition, the amount of testosterone
produced by existing Leydig cells is under the control of LH, which regulates
the expression of 17β-hydroxysteroid dehydrogenase.[133]
The amount of testosterone synthesized is regulated by the hypothalamic–

pituitary–testicular axis (see figure to the right).[134] When testosterone
levels are low, gonadotropin-releasing hormone (GnRH) is released by the
hypothalamus, which in turn stimulates the pituitary gland to release FSH
and LH. These latter two hormones stimulate the testis to synthesize
testosterone. Finally, increasing levels of testosterone through a negative
feedback loop act on the hypothalamus and pituitary to inhibit the release of
GnRH and FSH/LH, respectively.
Factors affecting testosterone levels may include:
Age: Testosterone levels gradually reduce as men age.[135][136] This

effect is sometimes referred to as andropause or late-onset
hypogonadism.[137]
Hypothalamic–pituitary–testicular
Exercise: Resistance training increases testosterone levels,[138]
axis
however, in older men, that increase can be avoided by protein
ingestion.[139] Endurance training in men may lead to lower testosterone
levels.[140]
Nutrients: Vitamin A deficiency may lead to sub-optimal plasma testosterone levels.[141] The secosteroid vitamin D
in levels of 400–1000 IU/d (10–25 µg/d) raises testosterone levels.[142] Zinc deficiency lowers testosterone
levels[143] but over-supplementation has no effect on serum testosterone.[144]
Weight loss: Reduction in weight may result in an increase in testosterone levels. Fat cells synthesize the enzyme
aromatase, which converts testosterone, the male sex hormone, into estradiol, the female sex hormone.[145]
However no clear association between body mass index and testosterone levels has been found.[146]
Miscellaneous: Sleep: (REM sleep) increases nocturnal testosterone levels.[147] Behavior: Dominance challenges
can, in some cases, stimulate increased testosterone release in men.[148] Drugs: Natural or man-made
antiandrogens including spearmint tea reduce testosterone levels.[149][150][151] Licorice can decrease the
production of testosterone and this effect is greater in females.[152]
Distribution
The plasma protein binding of testosterone is 98.0 to 98.5%, with 1.5 to 2.0% free or unbound.[153] It is bound 65% to
sex hormone-binding globulin (SHBG) and 33% bound weakly to albumin.[154]
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Plasma protein binding of testosterone and dihydrotestosterone
Compound Group Level (nM) Free (%) SHBG (%) CBG (%) Albumin (%)
Adult men 23.0 2.23 44.3 3.56 49.9
Adult women
Testosterone Follicular phase 1.3 1.36 66.0 2.26 30.4
Luteal phase 1.3 1.37 65.7 2.20 30.7
Pregnancy 4.7 0.23 95.4 0.82 3.6
Adult men 1.70 0.88 49.7 0.22 39.2
Adult women
Dihydrotestosterone Follicular phase 0.65 0.47 78.4 0.12 21.0
Luteal phase 0.65 0.48 78.1 0.12 21.3
Pregnancy 0.93 0.07 97.8 0.04 21.2
Sources: [153][155]
Metabolism
Both testosterone and 5α-DHT are
metabolized mainly in the liver.
[2][156] Approximately 50% of
testosterone is metabolized via
conjugation into testosterone
glucuronide and to a lesser extent
testosterone sulfate by
glucuronosyltransferases and
sulfotransferases, respectively.[2] An
additional 40% of testosterone is
metabolized in equal proportions
into the 17-ketosteroids androsterone
and etiocholanolone via the
combined actions of 5α- and 5β-
reductases, 3α-hydroxysteroid
dehydrogenase, and 17β-HSD, in that
order.[2][156][157] Androsterone and
etiocholanolone are then
glucuronidated and to a lesser extent
sulfated similarly to testosterone.
[2][156] The conjugates of testosterone
and its hepatic metabolites are
released from the liver into
circulation and excreted in the urine
and bile.[2][156][157] Only a small
12 of 34 28/11/2019, 23:49
fraction (2%) of testosterone is

Testosterone metabolism in humans
excreted unchanged in the urine.[156]
In the hepatic 17-ketosteroid

pathway of testosterone metabolism,
testosterone is converted in the liver
by 5α-reductase and 5β-reductase
into 5α-DHT and the inactive 5β-
DHT, respectively.[2][156] Then, 5α-
DHT and 5β-DHT are converted by
3α-HSD into 3α-androstanediol and
3α-etiocholanediol, respectively.
[2][156] Subsequently, 3α-
androstanediol and 3α-
etiocholanediol are converted by 17β-
HSD into androsterone and
etiocholanolone, which is followed by
their conjugation and excretion.
[2][156] 3β-Androstanediol and 3β-
etiocholanediol can also be formed in
this pathway when 5α-DHT and 5β-
DHT are acted upon by 3β-HSD
instead of 3α-HSD, respectively, and
they can then be transformed into
epiandrosterone and
epietiocholanolone, respectively.
[158][159] A small portion of
approximately 3% of testosterone is
reversibly converted in the liver into Testosterone metabolism in humans. Conjugation (sulfation and
androstenedione by 17β-HSD.[157] glucuronidation) occurs both with testosterone and with all of the other
steroids that have one or more available hydroxyl (-OH) groups in this
In addition to conjugation and the diagram.
17-ketosteroid pathway, testosterone
can also be hydroxylated and
oxidized in the liver by cytochrome P450 enzymes, including CYP3A4, CYP3A5, CYP2C9, CYP2C19, and CYP2D6.[160]
6β-Hydroxylation and to a lesser extent 16β-hydroxylation are the major transformations.[160] The 6β-hydroxylation of
testosterone is catalyzed mainly by CYP3A4 and to a lesser extent CYP3A5 and is responsible for 75 to 80% of
cytochrome P450-mediated testosterone metabolism.[160] In addition to 6β- and 16β-hydroxytestosterone, 1β-, 2α/β-,
11β-, and 15β-hydroxytestosterone are also formed as minor metabolites.[160][161] Certain cytochrome P450 enzymes
such as CYP2C9 and CYP2C19 can also oxidize testosterone at the C17 position to form androstenedione.[160]
Two of the immediate metabolites of testosterone, 5α-DHT and estradiol, are biologically important and can be formed
both in the liver and in extrahepatic tissues.[156] Approximately 5 to 7% of testosterone is converted by 5α-reductase
into 5α-DHT, with circulating levels of 5α-DHT about 10% of those of testosterone, and approximately 0.3% of
testosterone is converted into estradiol by aromatase.[3][156][162][163] 5α-Reductase is highly expressed in the male
reproductive organs (including the prostate gland, seminal vesicles, and epididymides),[164] skin, hair follicles, and
13 of 34 28/11/2019, 23:49
brain[165] and aromatase is highly expressed in adipose tissue, bone, and the brain.[166][167] As much as 90% of
testosterone is converted into 5α-DHT in so-called androgenic tissues with high 5α-reductase expression,[157] and due
to the several-fold greater potency of 5α-DHT as an AR agonist relative to testosterone,[168] it has been estimated that
the effects of testosterone are potentiated 2- to 3-fold in such tissues.[169]
Levels
Total levels of testosterone in the body are 264 to 916 ng/dL in men age 19 to 39 years,[170] while mean testosterone
levels in adult men have been reported as 630 ng/dL.[171] Levels of testosterone in men decline with age.[170] In women,
mean levels of total testosterone have been reported to be 32.6 ng/dL.[172][173] In women with hyperandrogenism, mean
levels of total testosterone have been reported to be 62.1 ng/dL.[172][173]
14 of 34 28/11/2019, 23:49
Testosterone levels in males and females
Total testosterone
Male Female
Stage Age range
Values SI units Values SI units
Premature (26–28 2.047–4.337 0.173–0.555

59–125 ng/dL 5–16 ng/dL
weeks) nmol/L nmol/L
Premature (31–35 1.284–6.871 0.173–0.763

Infant 37–198 ng/dL 5–22 ng/dL
weeks) nmol/L nmol/L
2.602–13.877 0.694–2.220
Newborn 75–400 ng/dL 20–64 ng/dL
nmol/L nmol/L
1–6 years ND ND ND ND
0.035–0.416
7–9 years 0–8 ng/dL 0–0.277 nmol/L 1–12 ng/dL
Child nmol/L
0.104–0.347
Just before puberty 3–10 ng/dL* <10 ng/dL* <0.347 nmol/L*
nmol/L*
0.035–1.666 0.069–1.214
10–11 years 1–48 ng/dL 2–35 ng/dL
nmol/L nmol/L
0.173–21.480 0.173–1.839
12–13 years 5–619 ng/dL 5–53 ng/dL
nmol/L nmol/L
Puberty
0.278–1.423
14–15 years 100–320 ng/dL 3.47–11.10 nmol/L 8–41 ng/dL
nmol/L
6.94–33.66 0.278–1.839
16–17 years 200–970 ng/dL* 8–53 ng/dL
nmol/L* nmol/L
12.15–37.48
≥18 years 350–1080 ng/dL* – –
nmol/L*
13.88–37.48
20–39 years 400–1080 ng/dL – –
nmol/L
12.15–30.88
40–59 years 350–890 ng/dL – –
nmol/L
Adult
12.15–24.98
≥60 years 350–720 ng/dL – –
nmol/L
0.347–1.873
Premenopausal – – 10–54 ng/dL
nmol/L
0.243–1.388
Postmenopausal – – 7–40 ng/dL
nmol/L
Bioavailable testosterone
Male Female
Stage Age range
0.007–0.045 0.007–0.045
1–6 years 0.2–1.3 ng/dL 0.2–1.3 ng/dL
nmol/L nmol/L
Child
0.007–0.079 0.007–0.146
7–9 years 0.2–2.3 ng/dL 0.2–4.2 ng/dL
nmol/L nmol/L
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Total testosterone
Male Female
Stage Age range
0.007–0.513 0.014–0.670
10–11 years 0.2–14.8 ng/dL 0.4–19.3 ng/dL
nmol/L nmol/L
0.010–8.082 0.038–0.541
12–13 years 0.3–232.8 ng/dL 1.1–15.6 ng/dL
nmol/L nmol/L
Puberty
0.274–9.525 0.087–0.652
14–15 years 7.9–274.5 ng/dL 2.5–18.8 ng/dL
nmol/L nmol/L
0.836–14.452 0.094–0.826
16–17 years 24.1–416.5 ng/dL 2.7–23.8 ng/dL
nmol/L nmol/L
≥18 years ND ND – –
0.066–0.791
Premenopausal – – 1.9–22.8 ng/dL
Adult nmol/L
0.055–0.662
Postmenopausal – – 1.6–19.1 ng/dL
nmol/L
Free testosterone
Male Female
Stage Age range
1–6 years 0.1–0.6 pg/mL 0.3–2.1 pmol/L 0.1–0.6 pg/mL 0.3–2.1 pmol/L
Child
Puberty 14–15 years 2.7–112.3 pg/mL 9.4–389.7 pmol/L 1.0–6.2 pg/mL 3.5–21.5 pmol/L
109.3–551.7
16–17 years 31.5–159 pg/mL 1.0–8.3 pg/mL 3.5–28.8 pmol/L
pmol/L
≥18 years 44–244 pg/mL 153–847 pmol/L – –
Adult Premenopausal – – 0.8–9.2 pg/mL 2.8–31.9 pmol/L
Postmenopausal – – 0.6–6.7 pg/mL 2.1–23.2 pmol/L
Sources: See template.
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Total testosterone levels in males throughout life
Life stage Tanner stage Age range Mean age Levels range Mean levels
Child Stage I <10 years – <30 ng/dL 5.8 ng/dL
Stage II 10–14 years 12 years <167 ng/dL 40 ng/dL
Stage III 12–16 years 13–14 years 21–719 ng/dL 190 ng/dL
Puberty
Stage IV 13–17 years 14–15 years 25–912 ng/dL 370 ng/dL
Stage V 13–17 years 15 years 110–975 ng/dL 550 ng/dL
Adult – ≥18 years – 250–1,100 ng/dL 630 ng/dL
Sources: [174][174][175][171][176][177]
Reference ranges for blood tests, showing adult male testosterone levels in light blue at center-left.
Measurement
Testosterone's bioavailable concentration is commonly determined using the Vermeulen calculation or more precisely
using the modified Vermeulen method,[178][179] which considers the dimeric form of sex-hormone-binding-
globulin.[180]
Both methods use chemical equilibrium to derive the concentration of bioavailable testosterone: in circulation
testosterone has two major binding partners, albumin (weakly bound) and sex-hormone-binding-globulin (strongly
bound). These methods are described in detail in the accompanying figure.
Dimeric sex-hormone- Two methods for

binding-globulin with its determining
testosterone ligands concentration of
bioavailable
testosterone.
17 of 34 28/11/2019, 23:49
History
A 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 Adolph Berthold (1803–1861).[181]
Research on the action of testosterone received a brief boost in 1889, when the Harvard professor Charles-Édouard
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 well-being were markedly restored
but the effects were transient,[182] and Brown-Séquard's hopes for the compound were dashed. Suffering the ridicule of
his colleagues, he abandoned his work on the mechanisms and effects of androgens in human beings.
In 1927, 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 recruited students willing to endure the tedious work of
extracting their isolates. In that year, Koch and his student, Lemuel McGee, derived 20 mg of a substance from a supply
of 40 pounds of bovine testicles that, when administered to castrated roosters, pigs and rats, remasculinized them.[183]
The group of Ernst Laqueur 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
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 1930s.
The Organon group in the Netherlands were the first to isolate the hormone,
identified in a May 1935 paper "On Crystalline Male Hormone from Testicles
(Testosterone)".[184] They named the hormone testosterone, from the stems of
testicle and sterol, and the suffix of ketone. The structure was worked out by
Schering's Adolf Butenandt, at the Chemisches Institut of Technical University
in Gdańsk.[185][186]
The chemical synthesis of testosterone from cholesterol was achieved in August

that year by Butenandt and Hanisch.[187] Only a week later, the Ciba group in
Zurich, Leopold Ruzicka (1887–1976) and A. Wettstein, published their
synthesis of testosterone.[188] These independent partial syntheses of
testosterone from a cholesterol base earned both Butenandt and Ruzicka the
joint 1939 Nobel Prize in Chemistry.[186][189] Testosterone was identified as
17β-hydroxyandrost-4-en-3-one (C19H28O2), a solid polycyclic alcohol with a
hydroxyl group at the 17th carbon atom. This also made it obvious that
Nobel Prize winner, Leopold
additional modifications on the synthesized testosterone could be made, i.e., Ruzicka of Ciba, a
esterification and alkylation. pharmaceutical industry giant
that synthesized testosterone.
The partial synthesis in the 1930s 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 Allan Kenyon's group[190] was able to demonstrate both anabolic and androgenic effects of testosterone
propionate in eunuchoidal men, boys, and women. The period of the early 1930s to the 1950s has been called "The
Golden Age of Steroid Chemistry",[191] and work during this period progressed quickly. Research in this golden age
proved that this newly synthesized compound—testosterone—or rather family of compounds (for many derivatives were
developed from 1940 to 1960), was a potent multiplier of muscle, strength, and well-being.[192]
18 of 34 28/11/2019, 23:49
Other animals
Testosterone is observed in most vertebrates. Testosterone and the classical nuclear androgen receptor first appeared in
gnathostomes (jawed vertebrates).[193] Agnathans (jawless vertebrates) such as lampreys do not produce testosterone
but instead use androstenedione as a male sex hormone.[194] Fish make a slightly different form called 11-
ketotestosterone.[195] Its counterpart in insects is ecdysone.[196] The presence of these ubiquitous steroids in a wide
range of animals suggest that sex hormones have an ancient evolutionary history.[197]
See also
List of androgens/anabolic steroids
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Further reading
Fargo KN, Pak TR, Foecking EM, Jones KJ (2010). "Molecular Biology of Androgen Action: Perspectives on
Neuroprotective and Neurotherapeutic Effects." (https://books.google.com/books?id=Y8jxd5vu6N8C&pg=PA127#
v=onepage&q&f=false). In Pfaff DW, Etgen AM (eds.). Molecular Mechanisms of Hormone Actions on Behavior.
Elsevier Inc. pp. 1219–1246. doi:10.1016/B978-008088783-8.00036-X (https://doi.org/10.1016%2FB978-00808878
3-8.00036-X). ISBN 978-0-12-374939-0.
Dowd NE (2013). "Sperm, testosterone, masculinities and fatherhood" (http://scholars.law.unlv.edu/nlj/vol13/iss2/8).
Nevada Law Journal. 13 (2): 8.
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Testosterone - Wikipedia https://en.wikipedia.

Testosterone is a steroid from the androstane class containing a

Measurement ChemSpider 5791 (http://www.chemspi

Examples include genital virilisation such as midline fusion, phallic Pharmacology

Aggression and criminality

aggressive behaviour in individuals.[85]

Immune system and inflammation

Steroid hormone activity

The amount of testosterone synthesized is regulated by the hypothalamic–

Factors affecting testosterone levels may include:

Age: Testosterone levels gradually reduce as men age.[135][136] This

Plasma protein binding of testosterone and dihydrotestosterone

Adult men 23.0 2.23 44.3 3.56 49.9

Testosterone Follicular phase 1.3 1.36 66.0 2.26 30.4

Luteal phase 1.3 1.37 65.7 2.20 30.7

Pregnancy 4.7 0.23 95.4 0.82 3.6

Adult men 1.70 0.88 49.7 0.22 39.2

Dihydrotestosterone Follicular phase 0.65 0.47 78.4 0.12 21.0

Luteal phase 0.65 0.48 78.1 0.12 21.3

Pregnancy 0.93 0.07 97.8 0.04 21.2

fraction (2%) of testosterone is

In the hepatic 17-ketosteroid

Testosterone levels in males and females

Premature (26–28 2.047–4.337 0.173–0.555

Premature (31–35 1.284–6.871 0.173–0.763

≥18 years 44–244 pg/mL 153–847 pmol/L – –

Adult Premenopausal – – 0.8–9.2 pg/mL 2.8–31.9 pmol/L

Postmenopausal – – 0.6–6.7 pg/mL 2.1–23.2 pmol/L

Sources: See template.

Total testosterone levels in males throughout life

Child Stage I <10 years – <30 ng/dL 5.8 ng/dL

Stage II 10–14 years 12 years <167 ng/dL 40 ng/dL

Stage V 13–17 years 15 years 110–975 ng/dL 550 ng/dL

Adult – ≥18 years – 250–1,100 ng/dL 630 ng/dL

Dimeric sex-hormone- Two methods for

The chemical synthesis of testosterone from cholesterol was achieved in August

Retrieved from "https://en.wikipedia.org/w/index.php?title=Testosterone&oldid=926657581"

This page was last edited on 17 November 2019, at 21:38 (UTC).

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