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Sex hormone
Sex hormone
Sex hormone
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Sex hormone
Drug class
Estradiol, an important estrogen sex hormone in both women and men
Class identifiers
SynonymsSex steroid; Gonadal steroid
UseVarious
Biological targetSex hormone receptors
Chemical classSteroidal; Nonsteroidal
Legal status
In Wikidata

Sex hormones, also known as sex steroids, gonadocorticoids and gonadal steroids, are steroid hormones that interact with vertebrate steroid hormone receptors.[1] The sex hormones include the androgens, estrogens, and progestogens. Their effects are mediated by slow genomic mechanisms through nuclear receptors as well as by fast nongenomic mechanisms through membrane-associated receptors and signaling cascades.[2] Certain polypeptide hormones including the luteinizing hormone, follicle-stimulating hormone, and gonadotropin-releasing hormone – each associated with the gonadotropin axis – are usually not regarded as sex hormones, although they play major sex-related roles.

Production

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Natural sex hormones are made by the gonads (ovaries or testicles),[3] by adrenal glands, or by conversion from other sex steroids in other tissue such as liver or fat.[4]

Production rates, secretion rates, clearance rates, and blood levels of major sex hormones
Sex Sex hormone Reproductive
phase 		Blood
production rate 		Gonadal
secretion rate 		Metabolic
clearance rate 		Reference range (serum levels)
SI units Non-SI units
Men Androstenedione
–
 2.8 mg/day 1.6 mg/day 2200 L/day 2.8–7.3 nmol/L 80–210 ng/dL
Testosterone
–
 6.5 mg/day 6.2 mg/day 950 L/day 6.9–34.7 nmol/L 200–1000 ng/dL
Estrone
–
 150 μg/day 110 μg/day 2050 L/day 37–250 pmol/L 10–70 pg/mL
Estradiol
–
 60 μg/day 50 μg/day 1600 L/day <37–210 pmol/L 10–57 pg/mL
Estrone sulfate
–
 80 μg/day Insignificant 167 L/day 600–2500 pmol/L 200–900 pg/mL
Women Androstenedione
–
 3.2 mg/day 2.8 mg/day 2000 L/day 3.1–12.2 nmol/L 89–350 ng/dL
Testosterone
–
 190 μg/day 60 μg/day 500 L/day 0.7–2.8 nmol/L 20–81 ng/dL
Estrone Follicular phase 110 μg/day 80 μg/day 2200 L/day 110–400 pmol/L 30–110 pg/mL
Luteal phase 260 μg/day 150 μg/day 2200 L/day 310–660 pmol/L 80–180 pg/mL
Postmenopause 40 μg/day Insignificant 1610 L/day 22–230 pmol/L 6–60 pg/mL
Estradiol Follicular phase 90 μg/day 80 μg/day 1200 L/day <37–360 pmol/L 10–98 pg/mL
Luteal phase 250 μg/day 240 μg/day 1200 L/day 699–1250 pmol/L 190–341 pg/mL
Postmenopause 6 μg/day Insignificant 910 L/day <37–140 pmol/L 10–38 pg/mL
Estrone sulfate Follicular phase 100 μg/day Insignificant 146 L/day 700–3600 pmol/L 250–1300 pg/mL
Luteal phase 180 μg/day Insignificant 146 L/day 1100–7300 pmol/L 400–2600 pg/mL
Progesterone Follicular phase 2 mg/day 1.7 mg/day 2100 L/day 0.3–3 nmol/L 0.1–0.9 ng/mL
Luteal phase 25 mg/day 24 mg/day 2100 L/day 19–45 nmol/L 6–14 ng/mL
Notes and sources
Notes: "The concentration of a steroid in the circulation is determined by the rate at which it is secreted from glands, the rate of metabolism of precursor or prehormones into the steroid, and the rate at which it is extracted by tissues and metabolized. The secretion rate of a steroid refers to the total secretion of the compound from a gland per unit time. Secretion rates have been assessed by sampling the venous effluent from a gland over time and subtracting out the arterial and peripheral venous hormone concentration. The metabolic clearance rate of a steroid is defined as the volume of blood that has been completely cleared of the hormone per unit time. The production rate of a steroid hormone refers to entry into the blood of the compound from all possible sources, including secretion from glands and conversion of prohormones into the steroid of interest. At steady state, the amount of hormone entering the blood from all sources will be equal to the rate at which it is being cleared (metabolic clearance rate) multiplied by blood concentration (production rate = metabolic clearance rate × concentration). If there is little contribution of prohormone metabolism to the circulating pool of steroid, then the production rate will approximate the secretion rate." Sources: See template.

Types

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In many contexts, the two main classes of sex hormones are androgens and estrogens, of which the most important human derivatives are testosterone and estradiol, respectively. Other contexts will include progestogens as a third class of sex steroids, distinct from androgens and estrogens.[5] Progesterone is the most important and only naturally occurring human progestogen. In general, androgens are considered "male sex hormones", since they have masculinizing effects, while estrogens and progestogens are considered "female sex hormones", since they have feminizing effects, although all types are present in each sex at different levels.[6]

Sex hormones include:

Synthetic sex steroids

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There are also many synthetic sex steroids.[7] Synthetic androgens are often referred to as anabolic steroids. Synthetic estrogens and progestins are used in methods of hormonal contraception. Ethinylestradiol is an example of a semi-synthetic estrogen. Specific compounds that have partial agonist activity for steroid receptors may require treatment by a steroid in one cell type, and, therefore, act like natural steroid hormones. These compounds are used in certain medical conditions. Some systemic effects of a particular steroid in the entire organism are only desirable within certain limits.[8]

See also

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References

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Revisions and contributorsEdit on WikipediaRead on Wikipedia

Sex hormone

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from Grokipedia
Sex hormones, also known as sex steroids or gonadal steroids, are a class of hormones primarily produced by the gonads—the ovaries in females and testes in males—that regulate sexual , reproductive function, and secondary sexual characteristics such as in females and in males. The three major classes of sex hormones are estrogens (e.g., , the most potent form), progestogens (e.g., progesterone), and androgens (e.g., testosterone), each exerting distinct effects: estrogens promote feminizing changes and support the , progestogens prepare the for , and androgens drive masculinizing traits and . These hormones are synthesized from through enzymatic pathways in the gonads, with smaller amounts produced by the adrenal glands and peripheral tissues. Their production and release are tightly regulated by the hypothalamic-pituitary-gonadal axis: the secretes (GnRH), which stimulates the to release (FSH) and (LH), in turn prompting the gonads to produce sex hormones and gametes. Levels fluctuate across the lifespan, surging during to initiate sexual maturation, stabilizing in adulthood to maintain , and declining with age, contributing to conditions like or andropause. Beyond reproduction, sex hormones influence a wide array of physiological processes, including bone density maintenance, muscle mass regulation, cardiovascular health, and even immune responses, with estrogens generally exerting protective effects on the heart and bones while androgens support muscle and production. Imbalances in sex hormones can lead to disorders such as , , or , highlighting their integral role in overall health.

Overview and Classification

Definition and Role

Sex hormones, also known as gonadal steroids or sex steroids, are a subclass of hormones synthesized from through enzymatic modifications, featuring a characteristic structure of four fused rings. These lipophilic molecules diffuse across cell membranes to bind intracellular receptors, acting as transcription factors that regulate in target tissues, thereby influencing a wide array of physiological processes. Unlike peptide hormones such as gonadotropins (e.g., and ), which are water-soluble and signal via cell surface receptors, sex hormones directly modulate nuclear activity without requiring second messengers. Their primary biological roles center on orchestrating sexual development, , and the establishment and maintenance of secondary characteristics. In , hormones drive the of reproductive organs and traits that distinguish males from females during critical developmental windows. They are essential for , promoting the production and maturation of gametes ( in males and ova in females) through coordinated cellular proliferation and differentiation. Additionally, hormones sustain the structural and functional integrity of reproductive tissues throughout adulthood, ensuring ongoing and hormonal balance. From an evolutionary perspective, sex hormones emerged prominently in vertebrates, where they facilitate the precise coordination of reproductive cycles, behaviors, and physiological adaptations necessary for successful and production. The major classes—estrogens, progestogens, and androgens—exemplify this functional diversity, with each type mediating distinct yet interconnected aspects of reproductive .

Historical Discovery

The understanding of sex hormones emerged from observations of the physiological effects of and in the 19th and early 20th centuries. In 1849, German physiologist Arnold Adolph Berthold published seminal experiments on capons ( roosters), noting that removal of the testes resulted in the loss of male secondary sexual characteristics, such as crowing, comb growth, and aggressive behavior, while these traits were preserved or restored if a testis was transplanted to another body site, suggesting the production of a diffusible substance influencing distant tissues. This work laid the groundwork for recognizing internal secretions, later termed hormones, in sexual development. Building on this, Austrian physiologist advanced the field in the early 1920s through experiments involving , ligation, and transplantation of gonads in and other animals, demonstrating that such interventions could alter sexual behavior and secondary characteristics, and proposing that gonadal extracts contained active principles responsible for these effects. The isolation of specific sex hormones marked a pivotal advancement in the 1920s and 1930s, driven by biochemical extraction techniques from urine and ovarian tissues. In 1929, American biochemist Edward Adelbert Doisy isolated estrone, the first , from the urine of pregnant women, confirming its role in inducing estrus in ovariectomized rats; independently achieved the same isolation that year from human pregnancy urine. Progesterone was crystallized in 1934 by George Washington Corner and Willard Myron Allen from sow corpora lutea, with independent isolations reported concurrently by Butenandt and colleagues from human pregnancy urine, Hartmann and Wettstein from pig ovaries, and Slotta, Ruschig, and Fels from the same source, establishing it as the progestational hormone essential for maintaining pregnancy. Testosterone followed in 1935, when Butenandt isolated it from bull urine and Ruzicka synthesized it from , elucidating its structure as an responsible for male characteristics. These discoveries earned significant recognition, including the 1939 shared by Butenandt and Ruzicka for their work on sex hormones, highlighting the chemical characterization of androgens and s. Doisy's contributions to estrogen isolation were later honored in his 1943 in Physiology or Medicine, shared for research, but underscored his foundational role in hormone biochemistry. In the mid-20th century, structural elucidation advanced through synthesis and early crystallographic methods. During and , total syntheses of estrone, progesterone, and testosterone were achieved by teams including Butenandt, Ruzicka, and others, confirming their steroid frameworks via degradation and reconstruction from precursors like . provided definitive structural insights, with and colleagues analyzing crystals of estrone, androsterone, testosterone, and progesterone in the late , revealing their planar ring systems and , which facilitated further biosynthetic understanding.

Biosynthesis and Production

Sites of Synthesis

Sex hormones are primarily synthesized in the gonads, with the ovaries in females producing estrogens and progestogens, and the testes in males producing androgens such as testosterone. In females, the ovarian granulosa and cells collaborate to generate estrogens like , while the is a key site for progesterone synthesis post-ovulation. In males, Leydig cells within the testes are the main locus for testosterone production. The adrenal glands contribute to sex hormone synthesis, albeit to a lesser extent than the gonads, primarily through the production of androgens such as dehydroepiandrosterone (DHEA) and in the zona reticularis. These adrenal androgens serve as precursors for further conversion into estrogens or more potent androgens in peripheral tissues, contributing less than 5% to total testosterone in adult males and up to 65% to testosterone production in premenopausal females during the (primarily via precursors). During , the emerges as a major site of sex hormone synthesis, producing large quantities of progesterone to maintain and estrogens such as to support fetal development. Placental production relies on precursors from maternal and fetal adrenals and gonads, with the cells facilitating this synthesis. Peripheral tissues also play a significant role in sex hormone production through local conversion rather than from . For instance, enzyme in converts adrenal and gonadal androgens into , contributing substantially to estrogen levels in postmenopausal women. Similar conversions occur in the liver, , and , where enzymes like transform testosterone into . While in humans the gonads dominate sex hormone production, species variations exist, particularly in adrenal contributions. In nonhuman , adrenal androgen secretion like DHEA is prominent and comparable to humans, but in non-primate mammals such as , adrenal output is minimal, with gonads providing nearly all . Gonadal synthesis across species is generally regulated by pituitary gonadotropins such as and .

Biochemical Pathways

Sex hormones are synthesized through a series of enzymatic reactions collectively known as steroidogenesis, starting from as the universal precursor. The process occurs primarily in the mitochondria and of steroidogenic cells, involving enzymes and hydroxysteroid dehydrogenases that catalyze , oxidation, and cleavage reactions. This pathway ensures the production of progestogens, androgens, and estrogens from shared intermediates. The initial and rate-limiting step involves the conversion of to via side-chain cleavage. This reaction is catalyzed by the mitochondrial side-chain cleavage (P450scc, also known as CYP11A1), which utilizes NADPH and molecular oxygen to cleave the eight-carbon side chain of , yielding and isocaproic acid. The equation for this transformation is: [cholesterol](/page/Cholesterol)+3O2+3NADPH→P450scc[pregnenolone](/page/Pregnenolone)+isocaproic acid+3NADP++3H2O\text{[cholesterol](/page/Cholesterol)} + 3 \text{O}_2 + 3 \text{NADPH} \xrightarrow{\text{P450scc}} \text{[pregnenolone](/page/Pregnenolone)} + \text{isocaproic acid} + 3 \text{NADP}^+ + 3 \text{H}_2\text{O}
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