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14.1: Development of the Male and Female Reproductive Systems - Biology

14.1: Development of the Male and Female Reproductive Systems - Biology


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The development of the reproductive systems begins soon after fertilization of the egg, with primordial gonads beginning to develop approximately one month after conception. Reproductive development continues in utero, but there is little change in the reproductive system between infancy and puberty.

Development of the Sexual Organs in the Embryo and Fetus

Females are considered the “fundamental” sex—that is, without much chemical prompting, all fertilized eggs would develop into females. To become a male, an individual must be exposed to the cascade of factors initiated by a single gene on the male Y chromosome. This is called the SRY (Sex-determining Region of the Y chromosome). Because females do not have a Y chromosome, they do not have the SRY gene. Without a functional SRY gene, an individual will be female.

In both male and female embryos, the same group of cells has the potential to develop into either the male or female gonads; this tissue is considered bipotential. The SRY gene actively recruits other genes that begin to develop the testes, and suppresses genes that are important in female development. As part of this SRY-prompted cascade, germ cells in the bipotential gonads differentiate into spermatogonia. Without SRY, different genes are expressed, oogonia form, and primordial follicles develop in the primitive ovary.

Soon after the formation of the testis, the Leydig cells begin to secrete testosterone. Testosterone can influence tissues that are bipotential to become male reproductive structures. For example, with exposure to testosterone, cells that could become either the glans penis or the glans clitoris form the glans penis. Without testosterone, these same cells differentiate into the clitoris.

Not all tissues in the reproductive tract are bipotential. The internal reproductive structures (for example the uterus, uterine tubes, and part of the vagina in females; and the epididymis, ductus deferens, and seminal vesicles in males) form from one of two rudimentary duct systems in the embryo. For proper reproductive function in the adult, one set of these ducts must develop properly, and the other must degrade. In males, secretions from sustentacular cells trigger a degradation of the female duct, called the Müllerian duct. At the same time, testosterone secretion stimulates growth of the male tract, the Wolffian duct. Without such sustentacular cell secretion, the Müllerian duct will develop; without testosterone, the Wolffian duct will degrade. Thus, the developing offspring will be female. For more information and a figure of differentiation of the gonads, seek additional content on fetal development.

Further Sexual Development Occurs at Puberty

Puberty is the stage of development at which individuals become sexually mature. Though the outcomes of puberty for boys and girls are very different, the hormonal control of the process is very similar. In addition, though the timing of these events varies between individuals, the sequence of changes that occur is predictable for male and female adolescents. As shown in the image below, a concerted release of hormones from the hypothalamus (GnRH), the anterior pituitary (LH and FSH), and the gonads (either testosterone or estrogen) is responsible for the maturation of the reproductive systems and the development of secondary sex characteristics, which are physical changes that serve auxiliary roles in reproduction.

The first changes begin around the age of eight or nine when the production of LH becomes detectable. The release of LH occurs primarily at night during sleep and precedes the physical changes of puberty by several years. In pre-pubertal children, the sensitivity of the negative feedback system in the hypothalamus and pituitary is very high. This means that very low concentrations of androgens or estrogens will negatively feed back onto the hypothalamus and pituitary, keeping the production of GnRH, LH, and FSH low.

As an individual approaches puberty, two changes in sensitivity occur. The first is a decrease of sensitivity in the hypothalamus and pituitary to negative feedback, meaning that it takes increasingly larger concentrations of sex steroid hormones to stop the production of LH and FSH. The second change in sensitivity is an increase in sensitivity of the gonads to the FSH and LH signals, meaning the gonads of adults are more responsive to gonadotropins than are the gonads of children. As a result of these two changes, the levels of LH and FSH slowly increase and lead to the enlargement and maturation of the gonads, which in turn leads to secretion of higher levels of sex hormones and the initiation of spermatogenesis and folliculogenesis.

In addition to age, multiple factors can affect the age of onset of puberty, including genetics, environment, and psychological stress. One of the more important influences may be nutrition; historical data demonstrate the effect of better and more consistent nutrition on the age of menarche in girls in the United States, which decreased from an average age of approximately 17 years of age in 1860 to the current age of approximately 12.75 years in 1960, as it remains today. Some studies indicate a link between puberty onset and the amount of stored fat in an individual. This effect is more pronounced in girls, but has been documented in both sexes. Body fat, corresponding with secretion of the hormone leptin by adipose cells, appears to have a strong role in determining menarche. This may reflect to some extent the high metabolic costs of gestation and lactation. In girls who are lean and highly active, such as gymnasts, there is often a delay in the onset of puberty.

Hormones of Puberty

During puberty, the release of LH and FSH from the anterior pituitary stimulates the gonads to produce sex hormones in both male and female adolescents.


Signs of Puberty

Different sex steroid hormone concentrations between the sexes also contribute to the development and function of secondary sexual characteristics. Examples of secondary sexual characteristics are listed in the table below.

Development of the Secondary Sexual Characteristics
MaleFemale
Increased larynx size and deepening of the voiceDeposition of fat, predominantly in breasts and hips
Increased muscular developmentBreast development
Growth of facial, axillary, and pubic hair, and increased growth of body hairBroadening of the pelvis and growth of axillary and pubic hair

As a girl reaches puberty, typically the first change that is visible is the development of the breast tissue. This is followed by the growth of axillary and pubic hair. A growth spurt normally starts at approximately age 9 to 11, and may last two years or more. During this time, a girl’s height can increase 3 inches a year. The next step in puberty is menarche, the start of menstruation.

In boys, the growth of the testes is typically the first physical sign of the beginning of puberty, which is followed by growth and pigmentation of the scrotum and growth of the penis. The next step is the growth of hair, including armpit, pubic, chest, and facial hair. Testosterone stimulates the growth of the larynx and thickening and lengthening of the vocal folds, which causes the voice to drop in pitch. The first fertile ejaculations typically appear at approximately 15 years of age, but this age can vary widely across individual boys. Unlike the early growth spurt observed in females, the male growth spurt occurs toward the end of puberty, at approximately age 11 to 13, and a boy’s height can increase as much as 4 inches a year. In some males, pubertal development can continue through the early 20s.


23.4: Development of the Male and Female Reproductive Systems

  • Contributed by Whitney Menefee, Julie Jenks, Chiara Mazzasette, & Kim-Leiloni Nguyen
  • Faculty at Reedley College, Butte College, Pasadena City College, & Mt. San Antonio College
  • Sourced from ASCCC Open Educational Resources Initiative

By the end of the section, you will be able to:

  • Explain how bipotential tissues are directed to develop into male or female sex organs
  • Name the rudimentary duct systems in the embryo that are precursors to male or female internal sex organs
  • Describe the hormonal changes that bring about puberty, and the secondary sex characteristics of men and women

The sperm has 24 hrs after ovulation to fertilize the ovum. Fertilization is defined as the combining of the 23 chromosomes from the sperm with the 23 chromosomes from the ovum. The fertilized egg, called a zygote, will undergo many rounds of cell division while the cilia inside the fallopian tube push it along. As the zygote divides, it is becomes a solid ball of 16 cells called a morula. The morula will continue dividing while hollowing out with a space in the center. This hollow ball of cells is now a blastocyst and will implant in the uterus. The development of the reproductive systems begins soon after fertilization of the egg, with primordial gonads beginning to develop approximately one month after conception. Reproductive development continues in utero, but there is little change in the reproductive system between infancy and puberty.

Watch this video Cell Division to see the early development after fertilization. What is the result if the cilia does not work?

Answer: The fertilized egg will remain in the fallopian tube resulting in a tubal pregnancy. The tube will eventually rupture, leading to internal bleeding and death if the bleeding continues.


BIO 140 - Human Biology I - Textbook

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Chapter 44

Development of the Male and Female Reproductive Systems

  • Explain how bipotential tissues are directed to develop into male or female sex organs
  • Name the rudimentary duct systems in the embryo that are precursors to male or female internal sex organs
  • Describe the hormonal changes that bring about puberty, and the secondary sex characteristics of men and women

The development of the reproductive systems begins soon after fertilization of the egg, with primordial gonads beginning to develop approximately one month after conception. Reproductive development continues in utero, but there is little change in the reproductive system between infancy and puberty.

Development of the Sexual Organs in the Embryo and Fetus

Females are considered the &ldquofundamental&rdquo sex&mdashthat is, without much chemical prompting, all fertilized eggs would develop into females. To become a male, an individual must be exposed to the cascade of factors initiated by a single gene on the male Y chromosome. This is called the SRY (Sex-determining Region of the Y chromosome). Because females do not have a Y chromosome, they do not have the SRY gene. Without a functional SRY gene, an individual will be female.

In both male and female embryos, the same group of cells has the potential to develop into either the male or female gonads this tissue is considered bipotential. The SRY gene actively recruits other genes that begin to develop the testes, and suppresses genes that are important in female development. As part of this SRY-prompted cascade, germ cells in the bipotential gonads differentiate into spermatogonia. Without SRY, different genes are expressed, oogonia form, and primordial follicles develop in the primitive ovary.

Soon after the formation of the testis, the Leydig cells begin to secrete testosterone. Testosterone can influence tissues that are bipotential to become male reproductive structures. For example, with exposure to testosterone, cells that could become either the glans penis or the glans clitoris form the glans penis. Without testosterone, these same cells differentiate into the clitoris.

Not all tissues in the reproductive tract are bipotential. The internal reproductive structures (for example the uterus, uterine tubes, and part of the vagina in females and the epididymis, ductus deferens, and seminal vesicles in males) form from one of two rudimentary duct systems in the embryo. For proper reproductive function in the adult, one set of these ducts must develop properly, and the other must degrade. In males, secretions from sustentacular cells trigger a degradation of the female duct, called the Müllerian duct . At the same time, testosterone secretion stimulates growth of the male tract, the Wolffian duct . Without such sustentacular cell secretion, the Müllerian duct will develop without testosterone, the Wolffian duct will degrade. Thus, the developing offspring will be female. For more information and a figure of differentiation of the gonads, seek additional content on fetal development.

A baby&rsquos gender is determined at conception, and the different genitalia of male and female fetuses develop from the same tissues in the embryo. View the video linked to below to see a comparison of the development of structures of the female and male reproductive systems in a growing fetus. Where are the testes located for most of gestational time?

Further Sexual Development Occurs at Puberty

Puberty is the stage of development at which individuals become sexually mature. Though the outcomes of puberty for boys and girls are very different, the hormonal control of the process is very similar. In addition, though the timing of these events varies between individuals, the sequence of changes that occur is predictable for male and female adolescents. As shown in Figure 1, a concerted release of hormones from the hypothalamus (GnRH), the anterior pituitary (LH and FSH), and the gonads (either testosterone or estrogen) is responsible for the maturation of the reproductive systems and the development of secondary sex characteristics , which are physical changes that serve auxiliary roles in reproduction.

The first changes begin around the age of eight or nine when the production of LH becomes detectable. The release of LH occurs primarily at night during sleep and precedes the physical changes of puberty by several years. In pre-pubertal children, the sensitivity of the negative feedback system in the hypothalamus and pituitary is very high. This means that very low concentrations of androgens or estrogens will negatively feed back onto the hypothalamus and pituitary, keeping the production of GnRH, LH, and FSH low.

As an individual approaches puberty, two changes in sensitivity occur. The first is a decrease of sensitivity in the hypothalamus and pituitary to negative feedback, meaning that it takes increasingly larger concentrations of sex steroid hormones to stop the production of LH and FSH. The second change in sensitivity is an increase in sensitivity of the gonads to the FSH and LH signals, meaning the gonads of adults are more responsive to gonadotropins than are the gonads of children. As a result of these two changes, the levels of LH and FSH slowly increase and lead to the enlargement and maturation of the gonads, which in turn leads to secretion of higher levels of sex hormones and the initiation of spermatogenesis and folliculogenesis.

In addition to age, multiple factors can affect the age of onset of puberty, including genetics, environment, and psychological stress. One of the more important influences may be nutrition historical data demonstrate the effect of better and more consistent nutrition on the age of menarche in girls in the United States, which decreased from an average age of approximately 17 years of age in 1860 to the current age of approximately 12.75 years in 1960, as it remains today. Some studies indicate a link between puberty onset and the amount of stored fat in an individual. This effect is more pronounced in girls, but has been documented in both sexes. Body fat, corresponding with secretion of the hormone leptin by adipose cells, appears to have a strong role in determining menarche. This may reflect to some extent the high metabolic costs of gestation and lactation. In girls who are lean and highly active, such as gymnasts, there is often a delay in the onset of puberty.

Figure 1: During puberty, the release of LH and FSH from the anterior pituitary stimulates the gonads to produce sex hormones in both male and female adolescents.

Signs of Puberty

Different sex steroid hormone concentrations between the sexes also contribute to the development and function of secondary sexual characteristics. Examples of secondary sexual characteristics are listed in Table 1.

Table 1: Development of the Secondary Sexual Characteristics

Male Female
Increased larynx size and deepening of the voice Deposition of fat, predominantly in breasts and hips
Increased muscular development Breast development
Growth of facial, axillary, and pubic hair, and increased growth of body hair Broadening of the pelvis and growth of axillary and pubic hair

As a girl reaches puberty, typically the first change that is visible is the development of the breast tissue. This is followed by the growth of axillary and pubic hair. A growth spurt normally starts at approximately age 9 to 11, and may last two years or more. During this time, a girl&rsquos height can increase 3 inches a year. The next step in puberty is menarche, the start of menstruation.

In boys, the growth of the testes is typically the first physical sign of the beginning of puberty, which is followed by growth and pigmentation of the scrotum and growth of the penis. The next step is the growth of hair, including armpit, pubic, chest, and facial hair. Testosterone stimulates the growth of the larynx and thickening and lengthening of the vocal folds, which causes the voice to drop in pitch. The first fertile ejaculations typically appear at approximately 15 years of age, but this age can vary widely across individual boys. Unlike the early growth spurt observed in females, the male growth spurt occurs toward the end of puberty, at approximately age 11 to 13, and a boy&rsquos height can increase as much as 4 inches a year. In some males, pubertal development can continue through the early 20s.

Chapter Review

The reproductive systems of males and females begin to develop soon after conception. A gene on the male&rsquos Y chromosome called SRY is critical in stimulating a cascade of events that simultaneously stimulate testis development and repress the development of female structures. Testosterone produced by Leydig cells in the embryonic testis stimulates the development of male sexual organs. If testosterone is not present, female sexual organs will develop.

Whereas the gonads and some other reproductive tissues are considered bipotential, the tissue that forms the internal reproductive structures stems from ducts that will develop into only male (Wolffian) or female (Müllerian) structures. To be able to reproduce as an adult, one of these systems must develop properly and the other must degrade.

Further development of the reproductive systems occurs at puberty. The initiation of the changes that occur in puberty is the result of a decrease in sensitivity to negative feedback in the hypothalamus and pituitary gland, and an increase in sensitivity of the gonads to FSH and LH stimulation. These changes lead to increases in either estrogen or testosterone, in female and male adolescents, respectively. The increase in sex steroid hormones leads to maturation of the gonads and other reproductive organs. The initiation of spermatogenesis begins in boys, and girls begin ovulating and menstruating. Increases in sex steroid hormones also lead to the development of secondary sex characteristics such as breast development in girls and facial hair and larynx growth in boys.


Development of the Male and Female Reproductive Systems

The development of the reproductive systems begins soon after fertilization of the egg, with primordial gonads beginning to develop approximately one month after conception. Reproductive development continues in utero, but there is little change in the reproductive system between infancy and puberty.

Development of the Sexual Organs in the Embryo and Fetus

Females are considered the “fundamental” sex—that is, without much chemical prompting, all fertilized eggs would develop into females. To become a male, an individual must be exposed to the cascade of factors initiated by a single gene on the male Y chromosome. This is called the SRY (Sex-determining Region of the Y chromosome). Because females do not have a Y chromosome, they do not have the SRY gene. Without a functional SRY gene, an individual will be female.

In both male and female embryos, the same group of cells has the potential to develop into either the male or female gonads this tissue is considered bipotential. The SRY gene actively recruits other genes that begin to develop the testes, and suppresses genes that are important in female development. As part of this SRY-prompted cascade, germ cells in the bipotential gonads differentiate into spermatogonia. Without SRY, different genes are expressed, oogonia form, and primordial follicles develop in the primitive ovary.

Soon after the formation of the testis, the Leydig cells begin to secrete testosterone. Testosterone can influence tissues that are bipotential to become male reproductive structures. For example, with exposure to testosterone, cells that could become either the glans penis or the glans clitoris form the glans penis. Without testosterone, these same cells differentiate into the clitoris.

Not all tissues in the reproductive tract are bipotential. The internal reproductive structures (for example the uterus, uterine tubes, and part of the vagina in females and the epididymis, ductus deferens, and seminal vesicles in males) form from one of two rudimentary duct systems in the embryo. For proper reproductive function in the adult, one set of these ducts must develop properly, and the other must degrade. In males, secretions from sustentacular cells trigger a degradation of the female duct, called the Müllerian duct . At the same time, testosterone secretion stimulates growth of the male tract, the Wolffian duct . Without such sustentacular cell secretion, the Müllerian duct will develop without testosterone, the Wolffian duct will degrade. Thus, the developing offspring will be female. For more information and a figure of differentiation of the gonads, seek additional content on fetal development.

A baby’s gender is determined at conception, and the different genitalia of male and female fetuses develop from the same tissues in the embryo. View this animation to see a comparison of the development of structures of the female and male reproductive systems in a growing fetus. Where are the testes located for most of gestational time?

Further Sexual Development Occurs at Puberty

Puberty is the stage of development at which individuals become sexually mature. Though the outcomes of puberty for boys and girls are very different, the hormonal control of the process is very similar. In addition, though the timing of these events varies between individuals, the sequence of changes that occur is predictable for male and female adolescents. As shown in (Figure), a concerted release of hormones from the hypothalamus (GnRH), the anterior pituitary (LH and FSH), and the gonads (either testosterone or estrogen) is responsible for the maturation of the reproductive systems and the development of secondary sex characteristics , which are physical changes that serve auxiliary roles in reproduction.

The first changes begin around the age of eight or nine when the production of LH becomes detectable. The release of LH occurs primarily at night during sleep and precedes the physical changes of puberty by several years. In pre-pubertal children, the sensitivity of the negative feedback system in the hypothalamus and pituitary is very high. This means that very low concentrations of androgens or estrogens will negatively feed back onto the hypothalamus and pituitary, keeping the production of GnRH, LH, and FSH low.

As an individual approaches puberty, two changes in sensitivity occur. The first is a decrease of sensitivity in the hypothalamus and pituitary to negative feedback, meaning that it takes increasingly larger concentrations of sex steroid hormones to stop the production of LH and FSH. The second change in sensitivity is an increase in sensitivity of the gonads to the FSH and LH signals, meaning the gonads of adults are more responsive to gonadotropins than are the gonads of children. As a result of these two changes, the levels of LH and FSH slowly increase and lead to the enlargement and maturation of the gonads, which in turn leads to secretion of higher levels of sex hormones and the initiation of spermatogenesis and folliculogenesis.

In addition to age, multiple factors can affect the age of onset of puberty, including genetics, environment, and psychological stress. One of the more important influences may be nutrition historical data demonstrate the effect of better and more consistent nutrition on the age of menarche in girls in the United States, which decreased from an average age of approximately 17 years of age in 1860 to the current age of approximately 12.75 years in 1960, as it remains today. Some studies indicate a link between puberty onset and the amount of stored fat in an individual. This effect is more pronounced in girls, but has been documented in both sexes. Body fat, corresponding with secretion of the hormone leptin by adipose cells, appears to have a strong role in determining menarche. This may reflect to some extent the high metabolic costs of gestation and lactation. In girls who are lean and highly active, such as gymnasts, there is often a delay in the onset of puberty.

Signs of Puberty

Different sex steroid hormone concentrations between the sexes also contribute to the development and function of secondary sexual characteristics. Examples of secondary sexual characteristics are listed in (Figure).

Development of the Secondary Sexual Characteristics
Male Female
Increased larynx size and deepening of the voice Deposition of fat, predominantly in breasts and hips
Increased muscular development Breast development
Growth of facial, axillary, and pubic hair, and increased growth of body hair Broadening of the pelvis and growth of axillary and pubic hair

As a girl reaches puberty, typically the first change that is visible is the development of the breast tissue. This is followed by the growth of axillary and pubic hair. A growth spurt normally starts at approximately age 9 to 11, and may last two years or more. During this time, a girl’s height can increase 3 inches a year. The next step in puberty is menarche, the start of menstruation.

In boys, the growth of the testes is typically the first physical sign of the beginning of puberty, which is followed by growth and pigmentation of the scrotum and growth of the penis. The next step is the growth of hair, including armpit, pubic, chest, and facial hair. Testosterone stimulates the growth of the larynx and thickening and lengthening of the vocal folds, which causes the voice to drop in pitch. The first fertile ejaculations typically appear at approximately 15 years of age, but this age can vary widely across individual boys. Unlike the early growth spurt observed in females, the male growth spurt occurs toward the end of puberty, at approximately age 11 to 13, and a boy’s height can increase as much as 4 inches a year. In some males, pubertal development can continue through the early 20s.

Chapter Review

The reproductive systems of males and females begin to develop soon after conception. A gene on the male’s Y chromosome called SRY is critical in stimulating a cascade of events that simultaneously stimulate testis development and repress the development of female structures. Testosterone produced by Leydig cells in the embryonic testis stimulates the development of male sexual organs. If testosterone is not present, female sexual organs will develop.

Whereas the gonads and some other reproductive tissues are considered bipotential, the tissue that forms the internal reproductive structures stems from ducts that will develop into only male (Wolffian) or female (Müllerian) structures. To be able to reproduce as an adult, one of these systems must develop properly and the other must degrade.

Further development of the reproductive systems occurs at puberty. The initiation of the changes that occur in puberty is the result of a decrease in sensitivity to negative feedback in the hypothalamus and pituitary gland, and an increase in sensitivity of the gonads to FSH and LH stimulation. These changes lead to increases in either estrogen or testosterone, in female and male adolescents, respectively. The increase in sex steroid hormones leads to maturation of the gonads and other reproductive organs. The initiation of spermatogenesis begins in boys, and girls begin ovulating and menstruating. Increases in sex steroid hormones also lead to the development of secondary sex characteristics such as breast development in girls and facial hair and larynx growth in boys.

Interactive Link Questions

A baby’s gender is determined at conception, and the different genitalia of male and female fetuses develop from the same tissues in the embryo. View this animation that compares the development of structures of the female and male reproductive systems in a growing fetus. Where are the testes located for most of gestational time?


Further Sexual Development Occurs at Puberty

Puberty is the stage of development at which individuals become sexually mature. Though the outcomes of puberty for boys and girls are very different, the hormonal control of the process is very similar. In addition, though the timing of these events varies between individuals, the sequence of changes that occur is predictable for male and female adolescents. As shown in Figure 15.3.1, a concerted release of hormones from the hypothalamus (GnRH), the anterior pituitary (LH and FSH) and the gonads (either testosterone or oestrogen) is responsible for the maturation of the reproductive systems and the development of secondary sex characteristics, which are physical changes that serve auxiliary roles in reproduction.

The first changes begin around the age of eight or nine when the production of LH becomes detectable. The release of LH occurs primarily at night during sleep and precedes the physical changes of puberty by several years. In pre-pubertal children, the sensitivity of the negative feedback system in the hypothalamus and pituitary is remarkably high. This means that very low concentrations of androgens or oestrogens will negatively feed back onto the hypothalamus and pituitary, keeping the production of GnRH, LH, and FSH low.

As an individual approaches puberty, two changes in sensitivity occur. The first is a decrease of sensitivity in the hypothalamus and pituitary to negative feedback, meaning that it takes increasingly larger concentrations of sex steroid hormones to stop the production of LH and FSH. The second change in sensitivity is an increase in sensitivity of the gonads to the FSH and LH signals, meaning the gonads of adults are more responsive to gonadotropins than are the gonads of children. As a result of these two changes, the levels of LH and FSH slowly increase and lead to the enlargement and maturation of the gonads, which in turn leads to secretion of higher levels of sex hormones and the initiation of spermatogenesis and folliculogenesis.

In addition to age, multiple factors can affect the age of onset of puberty, including genetics, environment, and psychological stress. One of the more important influences may be nutrition historical data demonstrate the effect of better and more consistent nutrition on the age of menarche in girls in the United States, which decreased from an average age of approximately 17 years of age in 1860 to the current age of approximately 12.75 years in 1960, as it remains today. Some studies indicate a link between puberty onset and the amount of stored fat in an individual. This effect is more pronounced in girls but has been documented in both sexes. Body fat, corresponding with secretion of the hormone leptin by adipose cells, appears to have a strong role in determining menarche. This may reflect the high metabolic costs of gestation and lactation. In girls who are lean and highly active, such as gymnasts, there is often a delay in the onset of puberty.

Figure 15.3.1. Hormones of puberty. During puberty, the release of LH and FSH from the anterior pituitary stimulates the gonads to produce sex hormones in both male and female adolescents.


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Clinical Urologic Endocrinology: Principles for Men's Health. Springer-Verlag London Ltd, 2013. p. 11-24.

Research output : Chapter in Book/Report/Conference proceeding › Chapter

T1 - Development of the male reproductive system

N2 - Male and female reproductive systems develop in close relation to the urinary tract. Until approximately 7 weeks gestation, the human embryo remains sexually bipotential. Subsequently, in males, testis-inducing factors cause differentiation from the default female phenotype. As the testis forms, testosterone and other androgens drive the formation of the external genitalia and internal male reproductive structures, while other testicular factors cause regression of female reproductive organ precursors. Androgens also play a role in the descent of the testicles from their origin in the upper abdomen. Germ cells enter an arrested phase of maturation in the fi rst trimester. A surge of testosterone in the neonatal period plays a role in testicular development, but it is not until the largest androgen surge of puberty that gonadarche occurs with the onset of spermatogenesis. In this chapter, we review the formation and maturation of the reproductive system, with an emphasis on hormonal factors and aspects relevant to clinical care of male reproductive patients.

AB - Male and female reproductive systems develop in close relation to the urinary tract. Until approximately 7 weeks gestation, the human embryo remains sexually bipotential. Subsequently, in males, testis-inducing factors cause differentiation from the default female phenotype. As the testis forms, testosterone and other androgens drive the formation of the external genitalia and internal male reproductive structures, while other testicular factors cause regression of female reproductive organ precursors. Androgens also play a role in the descent of the testicles from their origin in the upper abdomen. Germ cells enter an arrested phase of maturation in the fi rst trimester. A surge of testosterone in the neonatal period plays a role in testicular development, but it is not until the largest androgen surge of puberty that gonadarche occurs with the onset of spermatogenesis. In this chapter, we review the formation and maturation of the reproductive system, with an emphasis on hormonal factors and aspects relevant to clinical care of male reproductive patients.


Contents

Humans, many mammals, insects and other animals have an XY sex-determination system. Humans have forty-six chromosomes, including two sex chromosomes, XX in females and XY in males. The Y chromosome must carry at least one essential gene which determines testicular formation (originally termed TDF). A gene in the sex-determining region of the short arm of the Y, now referred to as SRY, has been found to direct production of a protein, testis determining factor, which binds to DNA, inducing differentiation of cells derived from the genital ridges into testes. [4] In transgenic XX mice (and some human XX males), SRY alone is sufficient to induce male differentiation. [5]

Other chromosomal systems exist in other taxa, such as the ZW sex-determination system in birds [6] and the XO system in insects. [7]

Environmental sex determination refers to the determination (and then differentiation) of sex via non-genetic cues like social factors, temperature, and available nutrients. In some species, such as the hermaphroditic clownfish, sex differentiation can occur more than once as a response to different environmental cues, [8] offering an example of how sex differentiation does not always follow a typical linear path.

There have been multiple transitions between environmental and genetic sex determination systems in reptiles over time, [9] and recent studies have shown that temperature can sometimes override sex determination via chromosomes. [10]

The early stages of human differentiation appear to be quite similar to the same biological processes in other mammals and the interaction of genes, hormones and body structures is fairly well understood. In the first weeks of life, a fetus has no anatomic or hormonal sex, and only a karyotype distinguishes male from female. Specific genes induce gonadal differences, which produce hormonal differences, which cause anatomic differences, leading to psychological and behavioral differences, some of which are innate and some induced by the social environment.

Various processes are involved in the development of sex differences in humans. Sexual differentiation in humans includes development of different genitalia and the internal genital tracts, breasts, body hair, and plays a role in gender identification. [11] [ better source needed ]

The development of sexual differences begins with the XY sex-determination system that is present in humans, and complex mechanisms are responsible for the development of the phenotypic differences between male and female humans from an undifferentiated zygote. [12] Atypical sexual development, and ambiguous genitalia, can be a result of genetic and hormonal factors. [13]

The differentiation of other parts of the body than the sex organ creates the secondary sex characteristics. Sexual dimorphism of skeletal structure develops during childhood, and becomes more pronounced at adolescence. Sexual orientation has been demonstrated to correlate with skeletal characters that become dimorphic during early childhood (such as arm length to stature ratio) but not with characters that become dimorphic during puberty—such as shoulder width. [14]

The first genes involved in the cascade of differentiation can differ between taxa and even between closely related species. For example: in zebrafish the first known gene to induce male differentiation is the amh gene, in tilapia it is tDmrt1, and in southern catfish it is foxl2. [15]

In fish, due to the fact that modes of reproduction range from gonochorism (distinct sexes) to self-fertilizing hermaphroditism (where one organism has functioning gonadal features of multiple sexes), sexual differentiation is complex. Two major pathways in gonochores exist: one with a nonfunctional intersexual phase leading to delayed differentiation (secondary), and one without (primary), where differences between the sexes can be noted prior to hatching. [3] Secondary gonochorists remain in the intersex phase until a biotic or abiotic cue directs development down one pathway. Primary gonochorism, without an intersex phase, follows classical pathways of genetic sex determination, but can still be later influenced by the environment. [3] Differentiation pathways progress, and secondary sex characteristics such as anal fin bifurcation and ornamentation typically arise at puberty. [15]

In birds, thanks to research on Gallus gallus domesticus, it has been shown that determination of sex is likely cell-autonomous, i.e. that sex is determined in each somatic cell independently of, or in conjunction with, the hormone signaling that occurs in other species. [16] Studies on gynandromorph chickens showed that the mosaicism could not be explained by hormones alone, pointing to direct genetic factors, possibly one or a few Z-specific genes such as double-sex or DMRT1. [16]

The most intensively studied species, such as fruit flies, nematodes, and mice, reveal that evolutionarily, sex determination/differentiation systems are not wholly conserved and have evolved over time. [9] Beyond the presence or absence of chromosomes or social/environmental factors, sexual differentiation can be regulated in part by complex systems like the ratio of genes on X chromosomes and autosomes, protein production and transcription, and specific mRNA splicing. [9]

Differentiation pathways can be altered at many stages of the process. Sex reversal, where the development of a sexual phenotype is redirected during embryonic development, happens in the initiation phase of gonadal sex differentiation. Even in species where there is a well-documented master regulator gene, its effects can be overridden by a downstream gene. [17]

Furthermore, hermaphrodites serve as examples of the flexibility of sexual differentiation systems. Sequential hermaphrodites are organisms that possess reproductive capabilities of one sex, and then that sex changes. [18] Differentiated gonadal tissue of the organism's former sex degenerates, and new sex gonadal tissue grows and differentiates. [8] Organisms that have the physiological capability to reproduce as a male and as a female at the same time are known as simultaneous hermaphrodites. Some simultaneous hermaphroditic organisms, like certain species of goby, have distinctive male and female phases of reproduction and can flip back and forth/"sex reverse" between the two. [19]

Socially-determined Edit

In some species, such as sequentially hermaphroditic clownfish, changes in social environment can lead to sexual differentiation or sex reversal, i.e. differentiation in the opposite direction. [8] In clownfish, females are larger than males, and in social groups, there is typically one large female, multiple smaller males, and undifferentiated juveniles. If the female is removed from the group, the largest male changes sex, i.e. the former gonad tissue degenerates and new gonad tissue grows. Furthermore, the pathway of differentiation in activated in the largest juvenile, which becomes male. [8]

Alternative morphs Edit

Sexual differentiation in a species does not have to produce one recognizable female type and one recognizable male type. In some species alternative morphs, or morphotypes, within one sex exist, such as flanged (larger than females, with large flap-like cheek-pads) and unflanged (about the same size as females, no cheek-pads) male orangutans, [20] and sometimes differences between male morphs can be more noticeable than differences between a male and a female within such species. [21] Furthermore, sexual selection can be involved in the development of different types of males with alternative reproductive strategies, such as sneaker and territorial males in dung beetles [22] or haremic males and pair-bonding males in the Nigerian cichlid fish P. pulcher. [15] [23] Sometimes alternative morphs are produced by genetic differences, and in other cases, the environment can be involved, demonstrating some degree of phenotypic plasticity. [24]

In many animals, differences in the exposure of a fetal brain to sex hormones are correlated with significant differences of brain structure and function, which correlate with adult reproductive behavior. [4] The causes of differences between the sexes are only understood in some species. Fetal sex differences in human brains coupled with early differences in experience may be responsible for sex differences observed in children between 4 years old and adolescence. [25]

Many individual studies in humans and other primates have found statistically significant sex differences in specific brain structures however, some studies have found no sex differences, some and meta-analyses have called into question the over-generalization that women and men's brains function differently. [26] Males and females statistically differ in some aspects of their brains, but there are areas of the brain which appear not to be sexually differentiated at all. Some scholars describe human brain variation not as two distinct categories, but as occupying a place on a maleness-femaleness continuum. [27]

In birds, hypotheses of male-female brain sex differences have been challenged by recent findings that differences between groups can be at least partially explained by the individual's dominance rank. [28] Furthermore, the behavioral causes of brain sex differences have been enumerated in studies of sex differences between different mating systems. For example, males of a polygynous vole species with intrasexual male competition have better spatial learning and memory than the females of their own species, but also better spatial learning and memory than all sexes of other closely related species that are monogamous thus the brain differences commonly seen as "sex differences" have been instead linked to competition. [29] Sexual selection does play a role in some species, though, as males who display more song behaviors are selected for by females–so some sex differences in bird song brain regions seem to have been evolutionarily selected for over time. [29]


The Gonads

Indifferent Stage

In the first stage of gonadal development, it is impossible to distinguish between the male and female gonad. Thus, it is known as the indifferent stage.

The gonads begin as genital ridges - a pair of longitudinal ridges derived from intermediate mesoderm and overlying epithelium. They initially do not contain any germ cells.

In the fourth week, germ cells begin to migrate from the endoderm lining of the yolk sac to the genital ridges, via the dorsal mesentary of the hindgut. They reach the genital ridges in the sixth week.

Simultaneously, the epithelium of the genital ridges proliferates and penetrates the intermediate mesoderm to form the primitive sex cords. The combination of germ cells and primitive sex cords forms the indifferent gonad - from which development into the testes or ovaries can occur.

Testes

In a male embryo, the XY sex chromosomes are present. The Y chromosome contains the SRY gene, which stimulates the development of the primitive sex cords to form testis (medullary) cords. The tunica albuginea, a fibrous connective tissue layer, forms around the cords.

A portion of the testis cords breaks off to form the future rete testis. The remaining cords contain two types of cells:

  • Germ cells
  • Sertoli cells (derived from the surface epithelium of the gland).

In puberty, these cords acquire a lumen and become the seminiferous tubules - the site within which sperm will be formed.

Located between the testis cords are the Leydig cells (derived from the intermediate mesoderm). In the eighth week, they begin production of testosterone - which drives differentiation of the internal and external genitalia.

Ovaries

In a female embryo, the XX sex chromosomes are present. As there is no Y chromosome, there is no SRY gene to influence development. Without it, the primitive sex cords degenerate and do not form the testis cords.

Instead, the epithelium of the gonad continues to proliferate, producing cortical cords. In the third month, these cords break up into clusters, surrounding each oogonium (germ cell) with a layer of epithelial follicular cells, forming a primordial follicle.

[caption align="aligncenter"] Fig 1 - Development of the male and female gonad from the indifferent gonad.[/caption]

Male Hormones

At the onset of puberty, the hypothalamus causes the release of FSH and LH into the male system for the first time. FSH enters the testes and stimulates the Sertoli cells to begin facilitating spermatogenesis using negative feedback, as illustrated in

Figure 24.14. LH also enters the testes and stimulates the interstitial cells of Leydig to make and release testosterone into the testes and the blood.

Testosterone , the hormone responsible for the secondary sexual characteristics that develop in the male during adolescence, stimulates spermatogenesis. These secondary sex characteristics include a deepening of the voice, the growth of facial, axillary, and pubic hair, and the beginnings of the sex drive.

Figure 24.14. Hormones control sperm production in a negative feedback system.

A negative feedback system occurs in the male with rising levels of testosterone acting on the hypothalamus and anterior pituitary to inhibit the release of GnRH, FSH, and LH. The Sertoli cells produce the hormone inhibin , which is released into the blood when the sperm count is too high. This inhibits the release of GnRH and FSH, which will cause spermatogenesis to slow down. If the sperm count reaches 20 million/ml, the Sertoli cells cease the release of inhibin, and the sperm count increases.


12.14 Reproductive and Developmental Toxicants

Reproductive toxicants are chemical, biohazardous, or physical agents that can impair the reproductive capabilities in men and/or women. Developmental toxicants interfere with proper growth or health of the child acting at any point from conception to puberty.

12.14.1 Adverse Effects Caused by Reproductive and Developmental Toxicants

  1. Genetic defects: Changes in germ cells that can be passed from one generation to the next, as well as genetic problems that arise at the point of fertilization (such as Down Syndrome). It is estimated that 20% of human malformations are due to inherited genetic defects that are present in the egg or sperm cell.
  2. Infertility: The inability of a couple to conceive after one year of regular intercourse without the use of contraceptives. One in twelve couples in the U.S. is infertile according to the Agency for Toxic Substances and Disease Registry (ATSDR). Hazardous exposures can cause infertility in males by interfering with hormones, damaging the testes (thus affecting sperm production), or by damaging the sperm leading to a reduction in sperm count, viability, motility, or functional capabilities. In women, the lack of ovulation or abnormal menstruation may cause infertility. This may be due to damage to the fallopian tubes, direct damage to the egg, or a change in the balance of sex hormones.
  3. Menstrual disorders: This effect has not been studied thoroughly however, any chemical that influences the balance of sex hormones could potentially cause menstrual irregularities.
  4. Impotence or decreased libido: Chemicals that affect the nervous system or the secretion of sex hormones have been shown to lower libido or alter sexual response in both males and females.
  5. Spontaneous abortion: Spontaneous abortion or miscarriage is the loss of the embryo or fetus before full term. Approximately 40% or more of all pregnancies end in spontaneous abortion (ATSDR). Spontaneous abortion may be caused when toxicants: a. Cause damage to the genetic material in the egg so that the embryo cannot survive b. Prevent the fertilized egg from implanting itself in the uterus or c. Directly affect the developing embryo or fetus, causing a lethal toxic effect.
  6. Stillbirth: Birth of a dead fetus. The death occurs late in the pregnancy or during birth.
  7. Birth defect: Physical abnormality or malformation present at birth, although it may not be detected. Two to three percent of all newborns have a serious birth defect (ATSDR). Approximately two-thirds of human birth defects have no known cause. The proportion that may be associated with exposure to hazardous substances is unknown. Teratogens are agents that cause birth defects to the embryo or fetus and usually occur during the first trimester.
  8. Low birth weight and premature birth: Agents can delay the growth or harm the health of the embryo or fetus without causing physical defects or death. Low birth weight is directly related to an increased risk of illness or death in the first year of life. Premature births are at risk for low birth weights and may suffer from the effects of immature organ systems.
  9. Childhood cancer: Carcinogens can affect the fetus by passing through the placenta to the fetus. These transplacetal carcinogens can later cause cancer in the child or young adult. Research in this area is limited however, work environments with exposures to metals, solvents, paints, and agricultural chemicals are of concern.
  10. Developmental disorders: Behavioral effects include hyperactivity, decreased attention span, slow learning ability, and in severe cases, mental retardation. These may be temporary or permanent effects. Due to limited studies, very few industrial chemicals that cause neurobehavioral defects have been identified.
  11. Breast milk and other exposures after birth: Some chemicals are stored in fat tissues and, since breast milk is rich in fat, infants can be exposed to these toxic chemicals. However, breastfeeding has many positive benefits that may outweigh the infant's risk of chemical exposure. Your healthcare provider should be consulted in these cases.
  12. Skin or clothing: Skin or clothing contaminated with chemicals can also be a route of exposure for infants and children at home. Using good work practices and leaving contaminated clothing at work will prevent this type of exposure.

12.14.2 Hazards of Reproductive and Developmental Toxicants

The greatest susceptibility to reproductive toxicants in women is usually during the first three to twelve weeks of pregnancy. During this period, a woman may not know that she is pregnant.

The nature and severity of the adverse effects depend on how much of the hazard the individual is exposed to, when and for how long, and how (by what route of exposure).

In order to appropriately recognize and control chemicals that may cause an increased risk of harm, three categories have been established. Toxicants that fall into Category 1 must be labeled Danger-Reproductive and Developmental Toxicant. The lab safety coordinator (ultimately the principal investigator or supervisor) is responsible for reviewing all lab chemicals and must determine whether any Category 1 chemicals are present. The lab safety coordinator also identifies any new Category 1 chemicals at the time of purchase. Pesticides have not been included in the tables.

Category 2 toxicants have sufficient animal evidence and limited human evidence and Category 3 have suspect or insufficient evidence.

12.14.3 Handling Procedures for Reproductive and Developmental Toxicants

Volatile reproductive toxicants must be handled inside a chemical fume hood to prevent inhalation exposure. Wear standard PPE (gloves, lab coat, and safety glasses) for handling reproductive toxicants. It is recommended that Section 12.11.8, Handling Procedure for Select Carcinogens, be followed when using Category 1 reproductive toxicants.

12.14.4 Storage of Reproductive and Developmental Toxicants

See Section 9, Proper Chemical Storage, for specific storage information. Reproductive toxicants should be labeled as such within the respective storage group.

12.14.5 Disposal of Reproductive and Developmental Toxicants

Refer to Chapter VI, Hazardous Waste Directory, for specific disposal information. Most reproductive toxicants will need to be labeled for collection by EH&S.

12.14.6 Emergency Response: Exposure

  1. Skin: Immediately remove affected clothing and flush contacted tissue with copious amounts of water for 15 minutes. If the skin is injured, proceed to the nearest hospital ER.
  2. Eye Contact: Rinse eyes with copious amounts of water for 15 minutes. Hold lids open while rinsing. Seek medical evaluation.

Complete an Accident-Illness Report Form as soon as possible and mail to EH&S at J3-200.

12.14.7 Emergency Response: Spills

Small spills can be cleaned with a universal absorbent while wearing safety goggles, gloves and a lab coat.

For large spills (>200 ml), evacuate the lab and call EH&S for clean-up.

12.14.8 Category 1 Reproductive and Developmental Toxicants: Sufficient Human Evidence

Category 1 agents are known human reproductive and/or developmental hazards. The scientific evidence to support this consists of sufficient epidemiologic evidence or human case studies along with strong supporting animal evidence for at least one adverse reproductive effect. Because the human data necessary to support this category are generally limited, there are currently few agents classified in this category. The potential reproductive effects listed are based on observation of toxic effects in studies of exposed humans or animals. Biohazardous and physical hazards are also included in this section.

Table 12.14.8.1 Category 1

Reported Adverse Effects

Female infertility, spontaneous abortion, growth retardation, developmental disorders

Male and female infertility, spontaneous abortion, birth defects, and growth retardation

Cancer chemotherapeutic drugs (e.g., methotrexate, cyclophosphamide)

Male and female infertility, spontaneous abortion, birth defects, growth retardation, some contaminate breast milk

Reduced male sex drive, male and female infertility, spontaneous abortion, growth retardation, menstrual disorders, breast milk contamination

Female infertility, spontaneous abortion, growth retardation, functional deficit

Male and female infertility, birth defects, developmental disorders

Male infertility, genetic defects, altered sex ratios

Male infertility, functional deficit, childhood cancer

Spontaneous abortion, male infertility, growth retardation, developmental disorders

Male infertility, developmental disorders, birth defects, low birth weight or premature births

Male and female infertility, spontaneous abortion, growth retardation, functional deficit, breast milk contamination

Mercury (organic such as methyl mercury)

Male infertility, birth defects, growth retardation, functional deficit, breast milk contamination

Low birth weight, spontaneous abortion, developmental disorders, breast milk contamination

Altered sex ratio, spontaneous abortions, impotence

Polychlorinated biphenyls (PCBs)

Male and female infertility, spontaneous abortion, growth retardation, breast milk contamination

Birth defects, developmental disorders, spontaneous abortions

Low birth weight, developmental disorders, birth defects, menstrual disorders, male and female infertility

Reported Adverse Effects

Spontaneous abortion, birth defects, growth retardation, developmental disorders, breast milk contamination

Growth retardation, liver disease in infected offspring, breast milk contamination

Functional deficit, childhood cancer

Adverse pregnancy outcomes

Rubella virus (German measles)

Birth defects, growth retardation, developmental disorders

Spontaneous abortion, birth defects, developmental disorders

Varicella-zoster virus (chicken pox and shingles)

Birth defects, growth retardation

Reported Adverse Effects

Heavy physical exertion (e.g., repetitive heavy lifting, stooping and/or climbing)

Spontaneous abortion, growth retardation

Male and female infertility, spontaneous abortion, birth defects, growth retardation, developmental disorders, childhood cancer

12.14.9 Category 2 Reproductive and Developmental Toxicants: Sufficient Animal Evidence/Limited Human Evidence

The agents listed in this category are probable or possible human reproductive hazards. The scientific evidence to support this includes data from experimental animal studies and/or limited human data. The minimum evidence necessary is a single, well-conducted study in one experimental animal species for one adverse reproductive effect. The potential reproductive effects listed are based on observation of toxic effects in studies of exposed animals and humans.

Table 12.14.9.1 Category 2

Acetaldehyde (with alcohol consumption)

Growth retardation, developmental disorders

Female infertility, birth defects, menstrual disorders

Male infertility, birth defects, reduced male sex drive

Anesthetic agents (e.g., nitrous oxide, halothane)

Male infertility, spontaneous abortion, birth defects, growth retardation, breast milk contamination

Spontaneous abortion, breast milk contamination

Antimony potassium tartrate

Premature birth, miscarriages, female infertility

Birth defects, spontaneous abortion

Female infertility, spontaneous abortion, birth defects, growth retardation, menstrual disorders

Reduced male sex drive, male infertility, female infertility

Male infertility, decreased libido, impotence, breast milk contamination

Male and female infertility, birth defects, growth retardation

Male and female infertility, birth defects, growth retardation, developmental disorders, breast milk contamination

Male and female infertility, genetic defects

Male and female infertility

Reported Adverse Effects (continued)

Spontaneous abortion, birth defects

Spontaneous abortion, birth defects

Birth defects, spontaneous abortion, male infertility

Dimethylformamide, N, N (DMF)

Spontaneous abortion, stillbirths, birth defects, female infertility

Male and female infertility, spontaneous abortion, birth defects, breast milk contamination

Male infertility, birth defects

Ethylene glycol monoethyl ether (EGEE)

Birth defects, female and male infertility, menstrual disorders

Ethylene glycol monomethyl ether (EGME)

Male infertility, birth defects, developmental disorders

Male and female infertility, spontaneous abortion, birth defects, growth retardation

Female infertility, spontaneous abortion

Female infertility, birth defects, menstrual disorders

Glycidyl ethers (e.g., allyl glycidyl ether, phenyl glycidyl ether)

Birth defects and male infertility among patients taking lithium

Reduced male sex drive, male infertility, breast milk contamination

Mercury (inorganic salts and metallic Hg)

Reduced male sex drive, male and female infertility, spontaneous abortion, birth defects, growth retardation, breast milk contamination

Male and female infertility, spontaneous abortion, developmental defects

Reported Adverse Effects (continued)

Reduced male sex drive, female infertility, birth defects

Spontaneous abortion, developmental disorders

Polyvinyl chloride (PVC resin)

Female infertility, spontaneous abortion, stillbirths

Spontaneous abortion, birth defects, female infertility, menstrual disorders, breast milk contamination

Birth defects, developmental disorders, spontaneous abortion, impotence, female infertility, menstrual disorders, breast milk contamination

Spontaneous abortions, female infertility, low fetal weights, birth defects

Male and female infertility, spontaneous abortion, breast milk contamination

Spontaneous abortion, birth defects, male infertility, menstrual disorders, breast milk contamination

Female infertility, spontaneous abortion, developmental disorders, birth defects, menstrual disorders, breast milk contamination

Male and female infertility, spontaneous abortion, birth defects

Reduced male sex drive, spontaneous abortion, birth defects, childhood cancer

Female infertility, birth defects, menstrual disorders, breast milk contamination

Reported Adverse Effects

Low atmospheric pressure (hypobaric)

Male infertility, growth retardation

High atmospheric pressure (hyperbaric)

Male infertility, birth defects

12.14.10 Category 3 Reproductive and Developmental Toxicants: Suspect/Insufficient Evidence

The agents in this category are possible or uncertain reproductive hazards. They are suspected to affect reproductive health but the data are insufficient. The existing data are from animal studies with no human data available.


Watch the video: Από τη σύλληψη στη γέννηση ελληνικοί υπότιτλοι (July 2022).


Comments:

  1. Maukus

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  2. Brenn

    I think this is a great idea



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