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The Concept of Male Reproductive Anatomy

  • University of Medical Sciences, ondo city, Nigeria

Abstract and Figures

The human reproductive system is made up of the primary and secondary organs, which helps to enhances reproduction. The male reproductive system is designed to produce male gametes and convey them to the female reproductive tract through the use of supportive fluids and testosterone synthesis. The paired testis (site of testosterone and sperm generation), scrotum (compartment for testis localisation), epididymis, vas deferens, seminal vesicles, prostate gland, bulbourethral gland, ejaculatory duct, urethra, and penis are the parts of the male reproductive system. The auxiliary organs aid in the maturation and transportation of sperm. Semen is made up of sperm and the secretions of the seminal vesicles, prostate, and bulbourethral glands (the ejaculate). Ejaculate is delivered to the female reproduc¬tive tract by the penis and urethra. The anatomy, embryology and functions of the male reproductive system are discussed in this chapter.
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The Concept of Male Reproductive
Oyovwi MegaObukohwo, Nwangwa EzeKingsley,
Rotu ArientareRume and EmojevweVictor
The human reproductive system is made up of the primary and secondary
organs, which helps to enhances reproduction. The male reproductive system is
designed to produce male gametes and convey them to the female reproductive
tract through the use of supportive fluids and testosterone synthesis. The paired
testis (site of testosterone and sperm generation), scrotum (compartment for
testis localisation), epididymis, vas deferens, seminal vesicles, prostate gland,
bulbourethral gland, ejaculatory duct, urethra, and penis are the parts of the male
reproductive system. The auxiliary organs aid in the maturation and transportation
of sperm. Semen is made up of sperm and the secretions of the seminal vesicles,
prostate, and bulbourethral glands (the ejaculate). Ejaculate is delivered to the
female reproduc¬tive tract by the penis and urethra. The anatomy, embryology and
functions of the male reproductive system are discussed in this chapter.
Keywords: AMH, TDF, SRY, SF, DHT etc.
. Introduction
Reproduction refers to the production of new offspring, also known as breeding
in animals. It includes a set of physiological processes (usually) that take place in
the female reproductive system with the association of behaviors and anatomical
structures that are necessary in order to ensure the birth of the next generation of
human, domestic, wild, and laboratory vertebrate organisms. Although these pro-
cesses take place within the female’s system, it is as a means of the fusion of haploid
gametes each from male (sperm cell) and female (ovum) termed, fertilization in
vertebrates. Testes, ductus deferens, epididymis, accessory glands, and penis make
up the male reproductive system [].
The males’ reproductive system functions mainly in the production, nourish-
ment and temporary storage of male gametes (spermatozoa), which is produced via
spermatogenesis. It produces androgens and estrogen through steroidogenesis []
and very importantly, connected to the organ of copulation (penis) which serves to
introduce semen containing spermatozoa into the female genital system via mating.
. Embryology of the reproductive system
The primordial germ cells have shifted from their previous extra embryonic
position to the gonadal ridges by the six weeks of development in both sexes,
Male Reproductive Anatomy
Figure 1.
Sexual differentiation in male and female.
where they are surrounded by the sex cords to form a pair of primitive gonads.
The forming gonad, whether chromosomally XX or XY, is potential until
this point. The current theory is that the development of an ovary or testis is
determined by the synchronized action of a series of genes that contribute to
the development of the ovary when there is no Y chromosome or there is no Y
testicular development. Unless a gene on the shooting arm of the Y named TDF
(testis defined factor) acts as a switch, the ovarian pathway is followed, diverting
development into the male pathway.
One of the leading current concerns in medical genetics is the search for the
main testis-determined gene. The medullary tissue forms traditional testes with
seminiferous tubules and Legdig cells in the presence of the Y chromosome that
become capable of androgen secretion under the stimulation of human chorionic
gonadotropin (HCG) from the placenta. Spermatogonia, produced by  or more
successive mitoses from the primordial germ cells, forms the walls of the seminifer-
ous tubules along with the supporting sertus cells. The gonad, by default, produces
an ovary if no Y chromosome is present; the cortex develops, the medulla regresses,
and oogonia starts to develop within follicles. Oogonia is obtained from primitive
germ cells by a sequence of approximately  mitoses, less than the number neces-
sary for spermatogenesis.
Oogonia joins meiosis  at about the end of the third month, but this process is
interrupted at a point called dictyotene, in which the cell persists until ovulation
happens several years later. Many of the oogonia degenerate before birth, and dur-
ing the years or so of sexual maturity of the female, only about  mature into
ovas. Thickenings in the ridges suggest the developing genital ducts, the mesoneph-
ric (formerly called Wolffian) and paramesonephric (formerly called mellerian)
ducts, while the primordial germ cells are migrating to the genital ridges. In the
male, androgen is released by the Legdig cells of the fetal testes, which stimulates
the mesonephric ducts to form the male genital ducts, and Sertoli cells produce
a hormone that suppresses paramesonephric duct formation. The mesonephric
ducts regress in the female (or in the non-gonadic embryo) and the parameso-
nephric ducts develop into the female duct system. The outer genitals consist of a
genital tubercle, paired labio scrotal swellings and paired urethra folds in the early
embryo. Under the influence of androgens, male external genitals develop from
The Concept of Male Reproductive Anatomy
this undifferentiated state or, in the absence of a testis, female external genitals
are produced regardless of whether an ovary is present. The male and the female
phenotype is as discuss below (Figure ).
. Male phenotype
• Fetal testicular cells secrete ample testosterone to increase blood concen-
trations to the same degree as those seen in adult males. Accumulation of
testosterone is increased by an additional influence of the gene product TDF
gene or SRY (sex determining region of the Y chromosome), which inhibits
aromatase production and prevents the conversion of testosterone to estrogens.
Testosterone promotes the growth and differentiation of the wolffian ducts
that develop into the internal male genital tracts.
• Sertoli cells in the newly differentiated seminiferous tubule secrete a glyco-
protein called antimullerian hormone (AMH) under the influence of the SRY
gene product and various transcription factors, inducing apoptosis of tubular
epithelial cells and atrophy or reabsorption of the mullerian ducts (which
would have become the female internal genital tract).
• The primitive structures that give rise to the outside genitalia in both sexes are
the urogenital sinus and genital tubarcle. Masculanization of these structures
relies on the secretion of testosterone by the fetal testis to form the penis,
scrotum and prostate gland. Those structures grow into the female external
genitalia unless stimulated by androgen. Differentiation is incomplete when
there is insufficient androgen in male embryos or too much androgen in female
embryos and the external genitals are unclear. Male external genitalia distinc-
tion relies on dilydrotestosterone rather than testosterone.
. Female phenotype
• Estrogen is secreted by the ovaries in gonadal females but not by testosterone
antimullerian hormone.
• Wolffian ducts cannot distinguish without testosterone.
• Mullerian is not suppressed without antimullerian ducts and thus develops into
the female internal genital tract.
. Male reproductive system
The human male reproductive system is a collection of organs that contribute
to the reproductive process situated outside the body and around a male’s pelvic
region. The key direct function of the male reproductive system is to supply the
ovum for fertilization by the male gamete or spermatozoa. The male reproductive
system is divided into four main compartments (as indicated in Figure ):
. e testis.
. Accessory ducts: is includes Epidydimis, Vas deferens, Ejaculatory Duct.
Male Reproductive Anatomy
. Accessory glands: Accessory glands are internal reproductive organs which
supply fluids that nourish the sperm cells and lubricate the duct system. ey
are the seminal vesicles, the the bulbourethral glands, and the prostate glands
(Cowper glands).
. Supporting structures which include the scrotum and the penis.
In mammals, paired testes, epididymides, ductus deferens, accessory sex glands
and penis are part of the male reproductive system. Tests perform two major roles
that are very crucial for life perpetuation, spermatogenesis and steroidogenesis
[]. Within the seminiferous tubules of the testis, spermatogenesis or spermatozoa
development takes place and steroidogenesis or testosterone synthesis occurs within
the interstitial compartment. Spermatogenesis takes place within the stratified
epithelium in the seminiferous tubules, while testosterone production takes place
inside the Leydig cells that are spread between the seminiferous tubules in a vascu-
lar, loose connective tissue in the interstitial compartment []. In determining male
secondary sexual characteristics, sperm development and fertility, testosterone,
developed by the Leydig testis cells, plays an important role [].
Epididymis is a single, long and extremely convoluted duct that connects the
vas deferens (a coiled duct that connects epididymis to the ejaculatory duct) to the
testicular efferent ducts. In the transport and storage of testicular spermatozoa,
Figure 2.
Typical structure of the male reproductive system.
The Concept of Male Reproductive Anatomy
epididymis plays an significant role. Epididymis is categorized in most mammals
into three distinct regions on the basis of its gross morphology; caput or head,
corpus or body and region of cauda or tail. The area of the corpus is thinner and it
joins the larger segments, caput and cauda. There is an additional canal in reptiles
between the testes and the epididymis head, which receives the numerous efferent
ducts. However, in both birds and mammals, this is missing []. A pseudostratified
epithelium surrounds the epididymis. The epithelium is divided from the connec-
tive tissue wall, which has smooth muscle cells, by a basement membrane. In the
epithelium, the main cell types are:
Principal cells: Columnar cells, with much of the epithelium in the basal cells.
They also have non-motile stereo cilia, which are long and branching in the head
region and shorter in the tail region, extending from the lumen to the basal lamina.
[]. Carnitine, sialic acid, glycoproteins, and ghycerylphosphorylchlorine are also
secreted into the lumen as well.
Basal cells: shorter, pyrmid-shaped cells that, before their apical surfaces enter
the lumen, touch the basal laminal but taper off []. These are known to be undif-
ferentiated primary cell precursors.
Apical cells: These are predominantly located in the head region []
Intraepithilial lymphocytes: distributed throughout the tissues.
Clear cell: Predominant in the tail region. The clear cells in the rat epididymis
are subdivided into two types and are concerned with the secretion of either glyco-
proteins or glylipoproteins. The blood epididymal barrier, constituted by the zona
occludens of the functional complexes at the apical ends of principal cells [] also
appears to play a vital role in maintaining a physiological millieu in the epididymal
canal suitable for sperm maturation.
Spermatozoa formed in the testis are functionally immature and as they migrate
through the epididymis they attain functional maturity. Epididymal epithelium
absorptive and secretory behavior helps to maintain a particular intraluminal
environment that is necessary for sperm maturation []. They transfer into the vas
deferens, where it is processed before ejaculation, as spermatozoa mature. Sperm
flows from the lower portion of the epididymis (which acts as a storage reservoir)
during ejaculation. They have not been activated by prostate gland products and are
unable to swim, but are transported inside the vas deferens by the peristaltic action
of muscle layers and are combined before ejaculation with the diluting fluids of the
seminal vessels and other accessory glands. There are some apical variations in the
epithelial cells of the epididymis that are sometimes referred to as stereo cillia, as
they appear like cilia under the light microscope. However, as electron microscopy
has shown that they are more similar to microvilli structurally and functionally,
some now refer to them as stereovilli. Stored sperm remain fertile for  to days,
but they disintegrate and the epididymis resorbs them if they become too mature
without being ejaculated. A thin tube approximately . centimeters long that
begins from the epididymis to the pelvic cavity is the vas deferens, also known as
the sperm duct. In order to transfer sperm, there are two ducts which connect the
left and right epididymis to the ejaculatory ducts. Each tube (in humans is about 
centimeters long and surrounded by smooth muscle.
The smooth muscle in the walls of the vas deferens contract reflexively during
ejaculation, thereby propelling the sperm forward. This is often referred to as peri-
stalsis. The sperm is passed into the urethra from the vas deferens, gathering secre-
tions from the male accessory sex glands, such as the seminal vesicles, the prostate
gland, and the bulbourethral glands that make up the majority of the semen. The
rate of fluid transfer by the vas deferens is not known in humans. The testes are
brought up close to the abdomen just before ejaculation, and fluid is rapidly trans-
ferred through the vas deferens into the area of the ejaculatory ducts and then into
Male Reproductive Anatomy
the prostatic urethra. Intravasal fluid is transported back into the epididymis after
ejaculation and even sometimes into the seminal vesicles []. Videoradiography
during ejaculation after vasography has recorded the retrograde transport of sperm
to the seminal vesicles. For some men after vasectomy, the return of sperm to the
seminal vesicles after ejaculation can help to explain the prolonged presence of
sperm in the ejaculate. The vas deferens can be obstructed or entirely missing,
causing male infertility (the latter a possible characteristic of cystic fibrosis).
Testicular sperm extraction (TESE), extracting sperm cells straight from the
testicles, will resolve it. Seminal vesicles (glandulae vesiculosae) or vesicular glands
are paired sac-like or simple tubular glands attached near the base of the bladder
to the vas deferens []. They are glands of approximately  to cm in length that
are extremely convoluted [, ]. Tubular alveoli with active secretary epithelium
are composed of seminal vesicles. The inner surface of the seminal vesicles consists
of tubules that form irregular diverticula and are thrown into an intricate system
of folds. The main portion of seminal fluid, the fluid that carries spermatozoa, is
around – of the seminal vesicle secretions []. A large proportion of the
substance that eventually becomes semen is secreted by the seminal vesicles. Dead
epithelial cell lipofuscin granules give the scretion its yellowish hue.
Seminal vesicles are highly androgen dependent and contain prostaglandins,
proteins, amino acids, citrate, fructose, flavins, enzymes, vitamin C and phospho-
ryl choline and their secretions are alkaline.
When processed in semen in the laboratory, the high fructose content provides
nutrient energy for the spermatozoa. Seminal vesicle secretions enhance sperm
capacity, increase sperm stability and help prevent sperm immune response in the
female reproductive tract []. Alkaline secretion helps to neutralize the vaginal
tract ‘s acidity, thus increasing sperm lifespan []. Secretion of the seminal vesicle in
semen also tends to improve sperm chromatin stability. In addition, from the fruc-
tose found in the seminal secretion, spermatozoa acquire their key energy source.
Prostate is a fibromuscular elastic, donut shaped gland covering the urethra
inferior to or at the urinary bladder neck []. A thin vascularized fibroelastic tissue
layer [] encapsulates the prostate. It is roughly ××cm in diameter and weighs
approximately g. From these endodermal cells, the glandular epithelium of the
prostate differentiates and the related mesenchyme differentiates into the prostate
‘s thick, solid and smooth muscle []. The primary function of the prostate is to
secrete milky fluid containing proteins and hormones that are part of the seminal
fluid produced by seminal vesicles. The prostate fluid is rich in phosphate acids, cit-
ric acid, fibrinolysin, antigen specific to the prostate, amylase, callikrein, zinc and
calcium, which are essential for spermatozoa to function normally. The secretions
of the prostate make up  percent of the amount of seminal fluid. The prostate
is an androgensensitive organ and relies on the presence or absence of circulating
androgens for growth and regression.
Two small glands situated on the sides of the urethra just below the prostate
gland are the bulbourethral glands, often referred to as Cowper glands. These
glands create a transparent, slippery fluid that directly empties the urethra. They
are homologous in female to the Bartholin glands []. Compound tubulo-alveolar
glands, each about the size of a pea in humans, are the bulbourethral glands [].
They are made of several lobules with a fibrous covering kept together. Each lobule
consists of a number of acini, lined by columnar epithelial cells, opening into a
duct that forms a single excretory duct joining the ducts of other lobules. This duct
is about .cm long and opens up at the base of the penis into the urethra. With
advancing age, the glands decline steadily in size. Each gland causes a clear, salty,
viscous secretion known as pre-ejaculate during sexual arousal. This fluid helps to
lubricate the urethra to move through spermatozoa, neutralizing traces of urethra
The Concept of Male Reproductive Anatomy
acidicurine [], and helps to flush out any residual urine or foreign matter. Since
there is no sperm in the preejaculate, it is possible for this fluid to absorb sperm,
stay in the urethral bulb from previous ejaculations, and conduct it until the next
ejaculation. Some amount of prostate specific antigen (PSA) is also produced by
the Cowper’s gland, and Cowper’s tumors can increase PSA to a level that makes
prostate cancer suspected [].
. Fundamental component of male reproductive anatomy
The male reproductive anatomy is divided into five components which are very
fundamental to human reproductive health. These include;
. Gonadal development: At eight weeks of gestation (perios of preganacy), Y
chromosomes synthesis of H-Y antigen occurs. In the male, this H-Y antigen
causes undierentiated sex glands to devlop into testes while in female, lack of
H-Y antigen causes undierentiated sex glands to develop into ovaries.
. Duct development: In this case, both sexes start out with two system such as
mullerian ducts which develops into fallopian tubes, uterus, inner vagina;
Wolan duct which develops into epididymis, vas dierens and seminal
vesicles. In the developmental processes, the male fetal leydig cells of the testes
secretes sucient testosterone as those seen in aduct men while the sertoli
cells of the testes secretes the antimullerian hormone (AMH). e testoster-
one (androgen) so secreted is responsible for male sex dierentiation during
embryogenesis (th and th weeks of pregnancy) and its accumulation is
enhanced by an additional eect of the testes determining factor (TDF) gene
or sex determining region of the Y chromosome (SRY) gene product which blocks
the expression of aromatase, thus preventing the conversion of testosterone
to estrogen. e testosterone thereby stimulate the growth and dierentia-
tion of the wolan ducts, which develop into the male internal genital tracts.
However, under the influence of the SRY gene product and specific transcrip-
tion factors, sertoli cells in newly dierentiated seminiferious tubule secretes
a glycoprotein called antimullerian hormone (AMH), which causes apoptosis
of tubular epithelia cells and atrophy or reabsorption of the mullerian ducts 
(Which would have become the female internal genital tract). Notwithstand-
ing, the downstream of genes that makes up the SRY gene product includes the
SOX and steriodogenesis factor (SF). ese classified products stimulate the
dierentiation of sertoli cells and leydigs in the testes and also in the formation
of tunica albuginea.
. External genital development: ere are two primitive structures of the re-
productive anatomy that give rise to the external genitalia in both sexes. is
includes the genital tubercle and the Urogenial sinus. However, the mascu-
linisation of these structures to form the penis, scrotum and prostate gland
depends on the secretion of testosterone by the fetal testes unless stimulated by
androgens; these structures develop into the female external genitalia (clitoris,
labia, vagina opening etc). When there is insucient androgen in male em-
bryos or too much androgen in female embryos, dierentiation is incomplete
and the external genitalia are ambiguous. Dierentiation of the masculine
external genitalia depends on the dehydrotesterone rather than testosterone.
e mechanism through which this occur is via the conversion of testosterone
into dihydrotestosterone (DHT) by an enzyme called α-reductase
Male Reproductive Anatomy
5 alpha reductase
testosterone dihydrotestosterone®
. Brain development: Sex hormone such as testosterone and estradiol exert their
influence during development of the fetus. Testosterone secreted into the
blood reaches the brain and gets converted into estradiol by an enzyme called
Aromatase. e estradiol is what actually help in the masculanization of the
human brain. In the female the estradiol secreyed by the ovaries binds to a par-
ticular protein called α-fetoprotein and therefore prevent its entering into the
brain to protect the female brain from being masculanized by estradiol.
testosterone estradiol
® ()
. Neural development: Neural development is one of the earliest systems to
begin and the last to be completed aer birth. is development generates
the most complex structure within the embryo and the long time period of
development means in utero insult during pregnancy may have consequences
to development of the nervous system. e early central nervous system begins
as a simple neural plate that folds to form a neural groove and then neural tube.
is early neural is initially open initially at each end forming the neuropores.
Failure of these opening to close contributes a major class of neural abnor-
malities (neural tube defects). Within the neural tube stem cells generate the
 major classes of cells that make the majority of the nervous system: neurons
and glia. Both these classes of cells dierentiate into many dierent types gen-
erated with highly specialized functions and shapes.
. The physio-anatomy of the testes
In adult males, the testis is a strong oval-shaped male gonad, about cm long
and .cm wide in size. Testes are located in the scrotum that regulates its tempera-
ture below the normal body temperature to approximately °C [, ]. There are
normally two testis, each weighing about –g with the right one usually slightly
larger and heavier than the left one weighing about + []. A testis (singular)
is surrounded by a saccular extension, called tunica vaginalis, of the peritoneum
inside the scrotum. Underneath the tunica vaginalis, Tunica albuginea is contained
and forms the testis’ white fibrous capsule []. Tunica albuginea is subsequently
thickened, assembling the testis mediastinum from which the fibrous septa pen-
etrates the testis and divides into about  to  wedge-shaped lobules.
There are one to four tightly coiled seminiferous tubules in each testicular lobule
where sperm is produced []. Testis seminiferous tubules consist of two main types
of cells, the germ cells and the supporting cells or Sertoli cells. In the seminiferous
epithelium, the Sertoli cells are uniformly distributed along with developing germ
cells and they nourish the germ cells during their growth. A basal lamina, which
includes peritubular myoid cells, lines the seminiferous tubule. Myoid cells consti-
tute a barrier of partial permeability by preventing large molecules from entering
the germinal epithelium. The close and gap junctions that exist between the adjacent
Sertoli cells, however, form the main exclusion barrier. The seminiferous epithelium
is divided into two distinct compartments by these inter-Sertoli cell junctions, called
the blood testis barrier: the basal and the adluminal compartments. Spermatogonia
and early spermatocytes live in the basal compartment and are readily available for
systemic circulation. The adluminal compartment is sequestered from the systemic
circulation, containing meiotic and post-meiotic spermatocytes, and is only exposed
The Concept of Male Reproductive Anatomy
to the components transported by Sertoli cells []. The undifferentiated spermato-
gonia that reside in the basal compartment of the seminiferous epithelium undergo
a series of mitotic divisions during the process of spermatogenesis to form primary
The primary spermatocyte is then moved to the adluminal compartment and
this requires comprehensive restructuring of the inter-Sertoli closed junctions.
The spermatocytes undergo two consecutive meiosis rounds in the adluminal
compartment to form mature haploid spermatids. In addition to offering physical
support to germ cells, Sertoli cells provide a special atmosphere in the adluminal
compartment, which is responsible for transporting sperm from the testis to the
epididymis by providing a specialized testis. Development factors and nutrients
that are essential for the survival of germ cells are important functions of the testis
[]. Germ cell variables, on the other hand, also play an important role in regulat-
ing the behavior of the Sertoli cells. For successful spermatogenesis, the interactions
between germ cells and Sertoli cells are important. The interstitial compartment
of the testis are made of steroid-secreting Leydig cells, blood and lymphatic ves-
sels, nerves, macrophages, fibroblasts and loose connective tissues. However, the
principal cells of this compartment are the Leydig cells of interstitial.
. Epithelial cells of the testes
. Sertoli cells (also called substantial cells)
Sertoli cells are large, irregularly shaped somatic cells. Sertoli cells are bound by
tight junctions to each other at their base. Sertoli cells, as shown by their close con-
tact, are essential to the formation of germ cells. A Sertoli cell can be connected to
as many as  to  spermatids. Sertoli cells assist in the spermiation process, where
the final detachment of mature spermatozoa into the seminiferous tubule lumen
takes place []. Excess cytoplasm resulting from the transition of spermatids to
spermatozoa, as well as damaged germ cells, are also targeted and phagocytized
by sertoli cells. Moreover, for germ cells, the Sertoli cells also provide structural
support and nutrition, secreting fluid. In the seminiferous epithelium of adult rats,
the columnar cells stretching from the basal to the luminal compartment are found
to occupy a volume of approximately – percent. Sertoli cell secretes inhibin,
which is a gonadal-origin nonsteroidal pituitary receptor []. The tight junctions
around the circumference of each tubule that lead to the blood-testis barrier were
created by a continuous layer of non-germinal Sertoli cells. Via the cytoplasm of
Sertoli cells, molecules from the blood join germinal cells. A protein called andro-
gen-binding protein is also secreted into the lumen of the seminiferous tubules by
Sertoli cells. The Sertoli cell cytoplasm spreads from the periphery to the tubule
lumen and envelops the developing germ cells. It helps to protect the seminiferous
tubules from immune attack; on the surface of T lymphocytes, the Sertoli cells gen-
erate FAS ligand that binds to the FAS receptor. In this way, by inducing apoptosis
of T lymphocytes, it avoids the immune attack of the developing sperm []. Sertoli
cells refer to the testes’ somatic cells, which are important for testes to develop and
also for spermatogenesis. Via direct interaction and regulation of the environment
inside the seminiferous tubules, these cells (Sertoli) promote the progression of
germ cells to spermatozoa. The blood testes barrier (BTB), which is produced near
the basement membrane by adjacent Sertoli cells, acts as a “gatekeeper” to pre-
vent harmful substances from reaching germ cells, especially during postmeiotic
spermatids. The BTB also divides the seminiferous epithelium into the basal and
luminal (apical) compartments to allow the growth of postmeiotic spermatids,
Male Reproductive Anatomy
namely spermiogenesis, to take place in the apical compartment behind the BTB in
a specialized microenvironment. The BTB also contributes to the immune privilege
status of the testis, at least in part, so that anti-sperm antibodies against antigens
that are transiently expressed during spermatogenesis are not produced []. Sertoli
cells have become incredibly difficult to remain morphologically stable because
during the  phases of the epithelial cycle they have a continuously evolving, three
dimensional relationship with growing germ cells. There have been many Sertoli
cell functions identified, most of which are directly related to the production and
movement of germ cells. These include ) the provision of structural support; ) the
production of an impermeable and immunological barrier; ) involvement in the
movement and spermation of germ cells; ) nutrition of germ cells through their
secretory products [].
. Leydig cells (or interstitial cells of the leydig)
Leydig cells are polygonal in form and are the main type of cell inside the
interstitial tissue where they are mostly located adjacent to the seminiferous tubules
and blood vessels. Other cell types, such as fibroblasts, macrophages and a limited
number of mast cells, are also present in the interstitial space, in addition to Leydig
cells. The primary source of testosterone in the systemic circulation of males is the
Leydig cells. The Leydig cell cytoplasm contains a lot of mitochondria, a granular
endoplasmic reticulum, lipid droplets and occasionally some protein crystals [].
Leydig cells do not have follicle stimulating hormone (FSH) receptors. Therefore
their growth is influenced indirectly rather than directly by the FSH. FSH acti-
vates the Sertoli cell development growth stimulators, which in turn stimulated
the growth of the Leydig cells that were growing. In addition, the proliferation of
developing Leydig cells can also be stimulated by the androgens. However, pro-
liferation and activity of these cells are reduced by the Estrogen receptors that are
present in the Leydig cells. Leydig cells have LH receptors, and inducing androgen
secretion through a cAMP-dependent mechanism is the main effect of the luteiniz-
ing hormone (LH). Testosterone is the primary product of Leydig cells, but dehy-
droepiandrosterone (DHEA) and androstenedione, two other androgens of less
biological activity, are also a product of Leydig cells []. However, now that human
testes live in the scrotum, they have adapted to this cooler climate and are unable to
generate sperm at the °C core body temperature. There are three mechanisms in
the scrotum to control test temperature:
Cremaster muscle: The cremaster muscle consists of strips that enmesh the sper-
matic cord of the internal abdominal obligue muscle. The cremaster contracts and
pulls the testicles closer to the body when it is cold to keep them warm. The cremas-
ter relaxes when it is warm and the testicles are suspended further from the body.
Darto muscle: A subcutaneous layer of smooth muscle is the darto muscle
(tunica dartos). When it is cold, it, too, contracts, and the scrotum becomes taut
and wrinkled. The scrotum ‘s teaching helps to keep the testes snugly against the
warm body and decreases the scrotums surface area, thus decreasing heat loss.
The pampiniform plexus is an extensive network of veins in the spermatic
cord from the testes that surround the testicular artery. These converge as they
pass through the inguinal canal to form the testicular vein, which emerges into
the pelvic cavity from the canal. Warm arterial blood will heat the testicles and
prevent spermatogenesis without the pampiniform plexus. However, by serving
as a countercurrent heat exchanger, the pampiniform plexus avoids this. Such a
process in the spermatic cord eliminates heat from the descending arterial blood,
so this blood is .c to .c cooler than the core body temperature by the time it
enters the testicles.
The Concept of Male Reproductive Anatomy
Most fish and amphibians do not have seminiferous tubules. The sperm is
instead formed in the spherical form known as sperm ampullae. These are seasonal
structures, which during the breeding season release their material and are then
reabsorbed by the body. Fresh sperm ampullae begin to develop and ripen before
the next breeding season. In higher vertebrates, with the same variety of cell types,
the ampullae are otherwise virtually similar to the seminiferous tubules.
. Testicular temperature regulation of testes
The testes perform best at temperature slightly lower than the core body tempera-
ture. At lower and higher temperatures, spermatogenesis is less effective[]. This is
possibly why the testicles are found outside of the body. To hold the tests at the optimum
temperature, there are various mechanisms [].
. Testicular development
The germ cells migrate from the yolk sac to the genital ridge during the rd week
of development after fertilization. In male embryos, testes develop from the genital
ridges from the th to the th week, and primordial germ cells migrate from the
wall of yolk sacs to the gonads. The Leydig cells of the developing testis are starting
to evolve under the influence of human chorionic gonadotropin. Testosterone is
secreted. The labioscrotal swellings merge at around week  to form the scrotum. In
order to form the epididymis, vas deferens and seminal vesicles, testosterone also
induces mesonephric (Wolfian) duct production []. The gubernaculum shortens
and pushes the testes, the deferent duct, and its vessels downward between the th
and the th week. The testes remain in the area of the inguinal canal between the
rd and th months so that they may enter into it. Under the control of the androgen
hormone, they enter the scrotum at roughly the time of birth. The vaginal process
appears as an outpouching of the parietal peritoneum at about weeks of develop-
ment. The testis stays for  to weeks at the beginning of the vaginal process,
the internal inguinal ring. This patent herniation mechanism is at least partially
dependent on the musculature of the abdominal wall to produce an elevated
intra-abdominal input. The patent processus vaginalis does not advance through
the inguinal canal if the abdominal muscles are unable to raise intra abdominal
pressure, and the testis may not descend into the scrotum. Each testis is formed
from three sources: First, in the th week of intrauterine life, the production of
testes becomes apparent. The medulla of the undifferentiated genital ridge, and the
cortex of which regresses, is the base of each testis. The proliferation of coelomic
mesothelium covering the medial surface of the mesonephric ridge forms the
genital ridge. From the proliferation of the endoderm of the dorsal wall of the hind
intestine, primitive sex cells or gonocytes are produced and appear in the genital
ridge through active dorsal and sephalic migration between the primitive dorsal
mesentery layers of the gut. From the surface of the genital ridge, multiple solid
cellular testis cords emerge and project into its interior. Within the testis cords,
primitive sex cells are inserted. A cellular plexus and the rete cord, which is located
near the blind ends of the mesonephric tubules, are connected by the inner ends
of the testis cords to form. Invading the genital ridge, the mesenchymal cells of
the mesonephrc ridge spread under the surface, later disconnecting the peripheral
ends of the testis cords from the surface. Tunica albuginea forms this portion of
the invaded cells. Some of the mesenchymal cells between the testis cords project
inwards and persist as a septa testis, and the interstitial cells are formed from the
Male Reproductive Anatomy
mesenchymal cells that are detached. The testis cords and rete cords are canalized
during the th month of intrauterine life and form the seminiferous tubules and the
rete testis, respectively. Secondly, efferent testis ductules are created to form the
proximal – of the persistent menosephric tubules that form secondary ties with
the rete testis. Epididymis and vas deferens are formed from the mesonephric duct
in the third channel. The epididymis precedes the testis into the processus vaginalis
at  to weeks of growth. These structures descend into the scrotum and are
fused with the scrotum ‘s posterior layers, providing an anchor that prevents the
movement of the testis. The vaginal process closes at  to weeks (full term),
preventing all contact between the peritoneum and the inguinal canal or scrotum.
A proximal remnant (or more than one remnant) may persist as a small appendage,
the appendix epididymis, as the mesonephric duct evolves into the epididymis.
Most frequently, this tissue is connected to the caput (most proximal and cephalad
portion) epididymis. Such an appendix can sometimes twist and become inflamed.
The paramesonephric structures (Müllerian) simultaneously regress under the
influence of the Müllerian inhibiting substance (MIS) secreted from the developing
testis by the Sertoli cells.
. Blood neurovascular supply of the testes
The survival of the cells in target organs depends on the delivery of nutrient-
rich, oxygenated blood and the removal of metabolic waste. In addition, neural
signaling is required for most organs to perform specific duties. In terms of the tes-
tes, each of the spherical reproductive organs is supplied by a rather basic bilateral
neurovascular network. The extensive vascular supply of the testes serves a variety
of functions in addition to supplying oxygen, nutrients, and eliminating waste from
the area. This is due to the organs temperature-sensitive functionality, as well as
their dual roles as endocrine glands and reproductive organs.
. Arterial supply
The testicular arteries are a pair of arterial structures on either side of the
abdominal aorta that branch straight from it. They arise at the level of the base of
the L-L vertebra from the anterolateral surface of the massive artery caudal to the
renal vessels. The right testicular artery travels inferolaterally, medial to the right
testicular vein and the proximal section of the right ureter, after crossing the infe-
rior vena cava anteriorly. The artery crosses the ureter anteriorly and continues its
inferior path on the body of the psoas major. The left testicular artery runs medial to
the testicular vein on the left side.
In comparison to the right testicular artery, it has a more vertical proximal path. It
also passes anteriorly through the left ureter. The common and external iliac vessels
are served by both the left and right testicular arteries. Only when they enter the
inguinal canal via the deep inguinal ring do they cross the external iliac vessels (at
which point the external iliac vessels become the femoral vessels). They run lateral
to the vas (ductus) deferens and its artery within the canal. The testicular artery
gives a branch to the epididymis after it enters the scrotum before bifurcating into
lateral and medial branches. These two branches further split to perforate the organ’s
material directly. There are also three noteworthy vascular anastomotic connections
formed with the testicular artery. Each of the cremasteric arteries originates on
the anteromedial side of its corresponding inferior epigastric artery (branch of the
external iliac artery) and forms an anastomosis with the testicular artery as it passes
through the spermatic cord (in the inguinal canal). The inferior vesical artery, which
The Concept of Male Reproductive Anatomy
is supplied by the anterior segment of the internal iliac artery, gives birth to the
ductus deferens artery. It also connects to the testicular artery via an anastomosis.
. Venous drainage
Around the testicular artery, a venous plexus is formed by a dense network of con-
nected veins. The pampiniform plexus is a network that travels cranially with cooler,
deoxygenated, nutrient-poor blood. The plexus’ branches continue to consolidate as it
leaves the scrotum and enters the spermatic cord, eventually becoming four branches.
Two branches join at the deep inguinal ring, on either side of the testicular artery. As
a result, each testicular artery has two valvular testicular veins that run alongside it to
their drainage locations. The two veins then merge to produce a single testicular vein
that flows laterally alongside the testicular artery across the psoas muscles anterior
surface. The neurovascular supply to the testes is definitely not a light topic, but
interactive anatomy can definitely make it easier to study. Each testicular vein crosses
its corresponding ureter on the front surface of the psoas muscles about the level of
the L vertebra. The left testicular vein then travels almost vertically to pierce the left
renal vein, passing between the testicular artery on the medial side and the ureter on
the lateral side. The right testicular vein, on the other hand, goes practically vertically
on the left side, then obliquely on the right side (also with the ureter lateral and the
testicular artery medial) before draining straight into the inferior vena cava.
. Innervation
The sympathetic nerve fibers that innervate the testes come from the T spinal
segment. The lesser splanchnic nerves carry them to the celiac ganglion, where they
synapse. The testicular artery is then followed along its route to its place of innerva-
tion by the post-ganglionic fibers. Sensory root fibers follow a similar path, passing
information to the T segment’s dorsal root ganglion cells. The testes’ tunica vagi-
nalis receives sensory innervation from the genital branch (L) of the genitofemoral
nerve (L, L) of the lumbar plexus.
. Lymphatic drainage
The testes are the only structures in the male external genitalia that do not leak
into the inguinal lymph nodes. Its lymphatics follow the path of the testicular veins
until they reach the para-aortic lymph nodes at the L vertebral level.
. Male reproductive functions
The male reproductive organs are specialized for the following functions:
• Spermatogenic function; for sperm production,
• maintainance and transport of sperm (the male reproductive cells and protec-
tive fluid semen)
• Sperm Discharge function; for discharging sperm inside the female reproduc-
tive tract.
• Hormonal function; for producing and secreting male sex hormones like
Male Reproductive Anatomy
. Spermatogenic functions
.. Semen
Sperm cells and secretions of the seminal vesicles, prostate, Cowper’s gland and,
perhaps, urothral glands are included in the fluid that is ejaculated in time of organ-
ism. It has a fixed gravity (.), a bright, opalescent fluid and a PH of .–.
of it. For each ejaculation, the approximate volume of semen is . to .ml after
several days of consistency []. The seminal vesicles contain the bulk of this secre-
tion or fluid (about  percent), and the prostate gland contributes the remainder
(about  percent). Components of seminal vesicle secretion include fructose,
phosphorylcholine, ergothioneine, ascorbic acid, flavins and prostaglandins, while
spermine, citric acid, cholesterol phospholipids, fibrinolysis, fibrinogenase, zinc,
and acid phosphate are components of prostate secretion. Semen is also known to
contain buffers (phosphate and bicarbonate) and hyaluronidase. The volume of the
semen containing sperm decreases rapidly with repeated ejaculation. The sperm
in human males ranges between  and million per millimeter in the ejaculated
semen (which accounts for about  of the semen volume), even though it takes
just only one sperm to fertilize the ovum. Human sperm moves through the female
genital tract at a rate of about nm/min and reaches the uterine tubes –min-
utes after copulation (sexual intercourse).
A sperm concentration below about  millimeter is termed oligospemia, and
is associated with decreased fertility. Various factors, including heat from a sauna
or hot tub, various prescription medications, lead and assenic poisoning and illicit
drugs such as marijuana, cocaine and anabolic steroids, may cause oligospermia.
In addition to low sperm counts, some men and women have antibodies against
sperm antigens as a cause of infertility (this is very common in men with vasec-
tomy). These antibodies do not tend to influence well being; however they decrease
fertility. Secretion from the epididgmins, seminal vesicles, prostate gland and
bulbourethral glands along with sperm composition makes up just  percent of the
semen or seminal fluidsperm, the rest is made up of accessory gland fluids. Semen
is over  water but contains many substance, most notably energy rich fructose,
the known vitamins which include Vitamins C and inositol and the trace elements
which include Calcium, Zinc, Magnesinm, copper and sulfur. Semen also contains
the highest concentration of prostaglandin in the body. The consistency of semen
varies from thick and viscous to almost watery fluid. Primordial germ cells are
the first cells destined to become semen. They are produced in the sac of the yolk,
a membrane connected with the embryo that is developing. They move into the
embryo itself in the fifth to sixth week of development and colonize the seminifer-
ous tubule, beyond the blood-test barrier (BTB). By mitosis, spermatogonia multi-
plies, producing two types of type A daughter cells and type B spermatogonia. Type
A cells remain beyond the barrier of blood tests and begin to multiply from puberty
until death. Therefore, men never exhaust their supply of gametes and typically
remain fertile in old age. Spermatogonia type B migrates closer to the lumen of the
tubule and differentiates into slightly large cells known as primary spermatocytes.
These cells must pass through the membrane of the blood testicles and travel into
the tubule lumen.
The tight junction between two sustentacular cells is usually dismantled ahead of
the primary spermatocyte, while a new tight junction is forms on the other side. The
primary spermatocyte undergoes mitosis , which gives rise to two equal- size, hap-
loid secondary spermatocytes. Each of these undergoes meiosis II, dividing into two
spermatid or a total of four for each spermatogomia. Each stage is a little bit closer to
the tubule than the previousr stages. All stages on the luminal side of the blood testies
The Concept of Male Reproductive Anatomy
barrier are bound to the sustentacular cells by the tight junctions and gap junction and
are closely enveloped in tendrils of the sustentacular cells. Throughout this meiotic
division, the daughter cell, remain connected to each other by means of narrow cyto-
plasmic bridges and do not completely separated. Hence, the rest of spermatogenesis is
called spermiogenesis. It does not involve further cell division, but a gradual transfor-
mation of each spermatid (immature sperm) into a matured spermatozoon.
.. Spermatogenesis
The cellular divisions and developmental changes that occur within the semi-
niferous tubules of the testes are termed spermatogenesis, and it consists of two
major parts (Figure ). In part , spermatocytogenesis occurs in which it starts with
spermatogonia which involve mitotic division of stem cells to form spermatocytes
that take place in the early stage, followed by meiosis where the number of chro-
mosomes is reduced to form spermatids. In part , spermiogenesis occurs in which
the spermatids are transformed in regards to metamorphic changes to sperm [].
Spermatogenesis is a highly organized but complex process and it normally continu-
ous throughout life []. The above description categories spermatogenesis into
Figure 3.
Showing the Microscopic anatomy of the seminiferous tubules.
Male Reproductive Anatomy
Figure 4.
Showing an overview of spermatogenesis (adapted from
major three divisions; spermatocytogenesis, meiosis and spermiogenesis respectively.
The process begins from spermatogonial stem cells that are found on the basement
membrane of the seminiferous tubules, which usually proliferate for self-renewal and
reproduced to a progeny of the differentiating spermatogenic cells such as () primary
spermatocytes, () secondary spermatocytes, () spermatids and () spermatozoa
[]. The spermatogonia are duplicated mitotic division, one of the duplicate member
called primary spermatocyte undergoes meiotic division in order to form secondary
spermatocytes. When the spermatogonia (which are a diploid primary spermatocyte)
complete the first meiosis, two daughter haploid cells will be produced, a result
which is known as secondary spermatocytes. By the end of the second (nd) meiotic
cell division, each of the two () secondary spermatocytes formed two () haploid
spermatids []. In the beginning, the spermatids will still pose the normal charac-
teristics of epithelioid cells, however, they differentiate and elongate into matured
spermatozoa. A matured spermatozoon comprises of a tail and a head which contains
a condensed nuclear material, a thin cytoplasm and a surrounding membranous layer
[]. The major features of spermiogenesis includes the formation of the acrosome
derived from the Golgi apparatus, condensation, elongation of the nucleus, formation
of the flagellum and extensive shedding of the cytoplasm of the spermiated, sperma-
tozoa consists of a head, middle piece and tail (Figure ) [].
.. Structure of mature spermatozoa and its membrane
The sperm consists of a head, a centerpiece, and a tail. The head comprises
nuclei surrounded by an acrosome of tightly packed chromatin. The acrosome
The Concept of Male Reproductive Anatomy
includes enzymes that are used for oocyte penetration. A special arrangement of
mitochondria spiraling around the middle part of the sperm is used for the produc-
tion of ATP for the passage of the sperm through the female reproductive tract.
Spermatozoa are driven by the tail or flagellum of the spermatozoa. Axoneme is
the microtubule and related protein bundle that forms the center of the flagellum
of eukaryotic sperm and is responsible for movement. Sperm cells and secretions
of the seminal vesicles, prostate, Cowper’s gland and, perhaps, urothral glands are
included in the fluid that is ejaculated in time of organism.
It has a fixed gravity (.), a bright, opalescent fluid and a PH of .–.
of it. For each ejaculation, the approximate volume of semen is . to .ml after
several days of consistency []. The seminal vesicles contain the bulk of this secre-
tion or fluid (about  percent), and the prostate gland contributes the remainder
(about  percent). Components of seminal vesicle secretion include fructose,
phosphorylcholine, ergothioneine, ascorbic acid, flavins and prostaglandins, while
spermine, citric acid, cholesterol phospholipids, fibrinolysis, fibrinogenase, zinc,
and acid phosphate are components of prostate secretion.
Semen is also known to contain buffers (phosphate and bicarbonate) and
hyaluronidase. The volume of the semen containing sperm decreases rapidly with
repeated ejaculation. The sperm in human males ranges between  and million
per millimeter in the ejaculated semen (which accounts for about  of the semen
volume), even though it takes just only one sperm to fertilize the ovum. Human
sperm moves through the female genital tract at a rate of about nm/min and
reaches the uterine tubes –minutes after copulation (sexual intercourse)
A sperm concentration below about  millimeter is termed oligospemia, and
is associated with decreased fertility. Various factors, including heat from a sauna
or hot tub, various prescription medications, lead and assenic poisoning and illicit
drugs such as marijuana, cocaine and anabolic steroids, may cause oligospermia. In
addition to low sperm counts, some men and women have antibodies against sperm
antigens as a cause of infertility (this is very common in men with vasectomy).
These antibodies do not tend to influence wellbeing, however they decrease fertility.
Secretion from the epididgmins, seminal vesicles, prostate gland and bulbourethral
glands along with sperm composition makes up just  percent of the semen or semi-
nal fluidsperm, the rest is made up of accessory gland fluids. Semen is over 
water but contains many substance, most notably energy rich fructose, the known
vitamins which include Vitamins C and inositol and the trace elements which
include Calcium, Zinc, Magnesinm, copper and sulfur. Semen also contains the
highest concentration of prostaglandin in the body. The consistency of semen varies
from thick and viscous to almost watery fluid. Primordial germ cells are the first
cells destined to become semen. They are produced in the sac of the yolk, a mem-
brane connected with the embryo that is developing. They move into the embryo
itself in the fifth to sixth week of development and colonize the seminiferous
tubule, beyond the blood-test barrier (BTB). By mitosis, spermatogonia multiplies,
producing two types of type A daughter cells and type B spermatogonia. Type A
cells remain beyond the barrier of blood tests and begin to multiply from puberty
until death. Therefore, men never exhaust their supply of gametes and typically
remain fertile in old age. Spermatogonia type B migrates closer to the lumen of the
tubule and differentiates into slightly large cells known as primary spermatocytes.
These cells must pass through the membrane of the blood testicles and travel into
the tubule lumen.
The tight junction between two sustentacular cells is usually dismantled ahead
of the primary spermatocyte, while a new tight junction is forms on the other side.
The primary spermatocyte undergoes mitosis , which gives rise to two equal- size,
haploid secondary spermatocytes. Each of these undergoes meiosis II, dividing
Male Reproductive Anatomy
into two spermatid or a total of four for each spermatogomia. Each stage is a little
bit closer to the tubule than the previousr stages. All stages on the luminal side of
the blood testies barrier are bound to the sustentacular cells by the tight junctions
and gap junction and are closely enveloped in tendrils of the sustentacular cells.
Throughout this meiotic division, the daughter cell, remain connected to each other
by means of narrow cytoplasmic bridges and do not completely separated. Hence,
the rest of spermatogenesis is called spermiogenesis. It does not involve further cell
division, but a gradual transformation of each spermatid (immature sperm) into a
matured spermatozoon (Figure ).
During sperm passage through the epididymis, spermatozoa collected or
derived from the testis do not show progressive motility or capacitate, but devel-
oped these abilities []. Dynamic morphological and metabolic changes leading
to the development of active sperm capable of fertilizing the ovum are referred
to as sperm maturation. These processes are called maturation. The comple-
tion of nuclear condensation and changes in the distribution and expression of
molecules on the surface of the sperm are all part of sperm maturational changes.
Phospholipid hydroperoxide glutathione peroxidase (GPx) may be used as an
alternative reductant to glutathione in the sperm nucleus by the thiol groups in
nuclear proteins. ROS lipid peroxide generation could provide GPx with a sub-
strate to drive the oxidation of these proteins and promote nuclear condensation,
while providing protection against oxidative DNA damage at the same time [].
By enhancing cyclic adenosine monophosphate (cAMP) synthesis and protein
phosphorylation at the time of ejaculation, reactive oxygen species could also be
involved in motility initiation []. For successful fertilization, the membrane
structure of spermatozoa plays a pivotal role, as both the acrosome reaction and
sperm-oocyte fusion are membrane-associated events; in fact, the spermatozoa
membrane lipids are essential for spermatozoa fluidity and flexibility. These
lipids, however, along with membrane proteins, are also the key substrates for
peroxidation that can cause serious sperm functional disorders []. High oxidant
concentrations have been shown to provoke sperm pathology such as ATP deple-
tion, leading to inadequate axonemal phosphorylation, lipid peroxidation and
loss of motility and viability. The adverse influence of reactive oxygen species
(ROS) is due to the sperm plasma membranes peroxidative damage. In addition,
in a high proportion of infertility patients, oxidative stress-mediated damage to
the sperm plasma membrane can account for defective sperm function observed.
In spermatozoa maturation, capacitation and the initiation of the gamete inter-
action process, ionic environment and ionic fluxes through the membrane are
extremely significant. In the mammalian sperm plasma membrane, various kinds
of ion channels are found, indicating a number of different functions in sperm
physiology and gamete interaction.
Figure 5.
Structure of a mature spermatozoon (adapted from [24]).
The Concept of Male Reproductive Anatomy
The plasma membrane integral enzymes in most animal cells are Na+/K+-ATPase
(E.C. ...) and Ca+-ATPase (E.C. ...) and are important components
involved in ionic homeostasis. Changes in the surrounding of the sperm membrane
and thus in fluidity change the activities of these enzymes, requiring the existence
of phospholipids closely linked to their structure. The Na+pump is a heteromeric
protein consisting of several isozymes and is not only responsible for maintaining
cell osmotic equilibrium, volume and pH, but also for maintaining the capacity
of the cell resting membrane and supplying chemical energy across the cell mem-
brane for the secondary Na+coupled transport of other ions, solutes and water.
The Ca+ pump, on the other hand, is responsible for the homeostasis of calcium
that is central to normal cell function. In particular, a distinctive Na+/K+-ATPase
isoform expression profile has been found in the mammalian testis with regard to
the Na+ pump. Sanchez et al. stated that the human Na+/K+-ATPase  isoform has
different functional properties and plays a primary role in the motility of sperm.
Sulphydryl (SH) containing enzymes are considered to be both ATPases and their
thiol groups may be the target for both nitric oxide (NO) and its derivatives such as
peroxynitrite (ONOO-). In fact, it has been clearly shown that NO and NOderived
reactive nitrogen species modulate the activity of different enzymes and can thus
damage cells, causing sperm dysfunction by increasing lipid peroxidation, complete
depletion of the sulphydryl group and formation of nitrotyrosine or by inactivating
proteins, damaging nucleic acids, which in turn leads to to alteration or distur-
bances in membrane structure and function. The development of several disease
states in humans is the accumulation of this oxidative damage and, in particular, the
progressive oxidation of sperm thiols to disulphides is involved in sperm chromatin
condensation and stabilization of the tail structure needed for the subsequent
initiation of motility. In particular, it has been revealed that peroxynitrite inhibi-
tion of Na+/K+-ATPase activity is followed by a reduction in the number of protein
thiol groups and a shift in the enzymes substrate dependency curve [, ]. This
means that the blockade of Na+/K+-ATPase ATPase SH-groups is responsible for its
inhibition []. The pattern of this inhibition is consistent either with the oxidation
of thiol groups directly involved in the binding of ATP but in a way that cannot be
resolved by raising the concentration of the substrate (‘noncompetitive’) or with
the oxidation of SH groups located outside the enzyme’s active site but essential for
the enzymes activity.
.. Capacitation and acrosome reaction
Capacitation is a morphological transition that spermatozoa are subjected to by
hyperactivation and acrosome reaction sequence to gain the capacity to fuse with
an ovum []. Sperm motility hyperactivation is characterized by a high amplitude,
asymmetrical sperm tail beating pattern and enables the sperm to enter the ovum
zone pellucida. It is accompanied by the acrosome reaction where acrosin and other
enzymes are released by the head of the mature spermatozoa to digest the cumulus
cells and break through the zona pellucida []. Research has shown that O-plays an
extremely important regulatory function in promoting both hyperactivated motion
and acrosome reaction induction [, ]. Increased membrane fluidity, increased
tyrosine phosphorylation, increased pH levels, increased intracellular cAMP, and
calcium influx are characterized by capacitation. Substances present in semen,
progesterone, peroxiredoxin- and other substances secreted by the oocyte cumulus
complex [] can regulate capacitation, but can also occur spontaneously under
sufficient in vitro conditions. Moreover, through the redox regulation of tyrosine
phosphorylation, ROS produced by mammalian spermatozoa can play a physiologi-
cally important role in driving the complex process of capacitation.
Male Reproductive Anatomy
The mechanism that support this redox-effect on protein tyrosine phosphoryla-
tion include a number of additional signal transduction stalls, such as sarcoma and
extracellular kinase regulated signal mediation pathways, stimulation of inhibition
of tyrosine phosphatase activity by cAMP generation. Capacitation is therefore
carried out by increasing membrane fluidity, cholesterol efflux, ion fluxes leading
to sperm membrane potential alteration, increased protein phosphorylation of
tyrosine, hyperactivation induction, and acrosome reaction. Reactive oxygen spe-
cies function alongside other factors including bicarbonate, membrane cholesterol
loss, and increased intracellular Ca+ resulting in activation of the cyclase of adenyl
(AC), leading to cAMP production and activation of protein kinase A (PKA) and
the phosphorylation of tyrosine proteins. Lewis and Aitken proposed that adenyl
cyclase is activated by superoxides, while Rivlin et al. [] proposed that cyclase
is activated by hydrogen peroxides that may substitute for bicarbonate. Increased
cAMP activates PKA, which activates tyrosine kinases and, by unknown mecha-
nisms, inhibits tyrosine phosphatassase (TP). The participation of PKA with the
PKA inhibitor (H) was confirmed. Hydrogen peroxide stimulates TK directly and
inhibits TP. The main driving force of capacitation and conduct to hyperactivation,
zone binding and acrosome reactions is the increase of the tyrosine phosphoryla-
tion induced by such changes []. The increase of fertilization by  percent by
induction of mild LPO using a mixture of ferrous ion and ascorbic acid was seen in
vitro studies performed on mouse sperm. The study shows that a strongly hydrogen
peroxide-induced OS activates sperm activity and improves fertilization rate.
Superoxide anion induces capacitation in incubation conditions by the effects of an
oxidase. Further stimulation of the development of ROS; superoxide anion, hydro-
gen peroxide induce the release from plasma of these cells of unesterified fatty acid.
.. Sperm abnormalities
Sperm anomalies, which are usually based on sperm concentration, motility, and
morphology, include: oligospermia (sperm concentration lesser than  million/ml).
This is supported by Iammarrone et al. [], which showed low conception rate in
human sperm counts with a concentration lesser than  million/ml. A complete lack
of spermatozoa in an ejaculate is termed azoospermia and such is found to accounts for
– percent of male infertility cases. Partial obstruction of sperm duct also influ-
enced sperm concentration []. Asthenospermia (poor sperm motility), is a condition
in which spermatozoa are too slow in movement, not able to strive in a straight line
along the cervical mucus within the female reproductive tract and or fertilize the egg.
When  or more sperm actively move in a straight line, the percentage motility is
said to be normal, and quality is at least average. In cases where percentage motility
is less than , the sperm the condition is as less qualitative. Genetic or otherwise
sperm defects may be responsible for sluggishly sperm movement and this may render
them incompetent of fertilizing the egg. Poor sperm motility associated with DNA
fragmentation can increase the risk of genetic diseases transmitted to offspring. Sperm
motility is rated in two ways: percentage of the total motility (general motility), or the
individual forward progressive sperm movement (progressive motility) []. The lat-
ter is a grade dependent on the pattern of the majority of motile sperm. It ranges from
null indicating (no movement) to four (suggesting excellent forward progression).
Notably, a sperm sample needs to have at least  progressive motility. Teratospermia
or morphologic abnormalities are usually categorized based location of the deformity
of a spermatozoon, whether it is on the head, neck (midpiece), or tail.
Primary and secondary anomalies are the most important classification scheme
types: primary abnormalities are structural defects in the location affecting head,
midpiece and tail. While the sperm was still inside the seminiferous epithelium of
The Concept of Male Reproductive Anatomy
the testis, a more primary serious defect is thought to originate while secondary
defects are considered less extreme and thought to occur during the passage through
the epididymis or by mishandling after ejaculation (sperm). The heterogeneous state
of teratozoospermia includes changes in the form of various components of sperm.
There is a strong connection between morphological defects and the potential for
sperm fertilization, since mature spermatozoa structures have the best organization
to serve specific functions. Teratozoospermia can therefore be considered to be a
mixture of morphological defects with associated sperm function impairments [].
.. Factors influencing spermatogenesis
The spermatogenesis process is highly sensitive to environmental fluctuations,
especially hormones and temperatures. In order to sustain the process, which is
accomplished by bidding testosterone with androgen binding protein present
in the seminiferous tubules, testosterone is needed at large local concentrations.
Testosterone is produced by interstitial cells that reside adjacent to the serminifer-
ous tubule, also referred to as ledig cells. In humans and certain other animals, the
seminiferous epithelium is susceptible to elevated temperatures and can be adversely
affected by temperatures as high as average body temperature; therefore, the testes
are found in a skin sack called the scrotum outside the body. At °C (Man) -°C
(mouse) below body temperature, the optimum temperature is preserved. This is
accomplished by controlling blood flow and by placing the cremasteric muscle and
dartos smooth muscle towards or away from the body heat. A nutritional deficien-
cies (such as vitamins B, E, and A), anabolic steriod, metals (Cadmium and lead),
X-ray exposure, dioxin, alcohol, drug toxicant and diseases of pathogens may also
adversely affect the rate of spermatogenesis [, ].
. Testicular steroidogenesis
For both spermatogenesis and the development of secondary sex characteristics,
steroidogenesis, which involved the production of testosterone (T) and dihydrotes-
tosterone (DHT) from cholesterol by a series of P enzymes in the Leydig testis
cells, is essential. The differentiation of the Wolffian ducts into the epididymides,
vasa deferentia, seminal vesicles, and the development of the levatorani-muscle
and bulbocavernosus gland (the LABC complex) is the responsibility of T in utero
(produced locally by the interstitial Leydig cells regulated by LH). DHT (produced
locally in the testis by T conversion using the -alpha-reductase enzyme) is respon-
sible for differentiating the genital tubercle from the external genitalia and the
urogenital sinus into the glands of the prostate and Cowper and for regression of
nipple anlagen in the male fetuses. According to the receptors to which they attach,
steroid hormones can be classified into five distinct groups: mineralocorticoids,
glucocorticoids, androgens, estrogen and progestagen. Cholesterol, the basic pre-
cursor for biosynthesis of all steroid hormones, is integrated by receptor-mediated
endocytosis into the Leydig cell from low-density lipoproteins or is synthesized
de novo from acetate within the cell. In cytoplasmic lipid droplets, cholesterol is
contained in an ester form and the number of droplets in Leydig cells is regarded to
be inversely proportional to the rate of androgen synthesis []. LH-induced choles-
terol ester hydrolase activation hydrolyzes cholesterol ester during steroidogenesis,
which is transported into the mitochondria of Leydig cells. The StAR protein is used
to transport cholesterol from the outside to the inner mitochondrial membrane.
The exact mechanism by which cholesterol is transported by StAR protein to the
mitochondria, however, remains uncertain. StAR protein is regulated acutely, and
protein expression is critically dependent on stimulation of trophic hormones (e.g.
Male Reproductive Anatomy
LH and ACTH). This makes it sensitive to toxicants from the environment: several
xenobiotics [e.g. -tert-octylphenyl and pesticides Lindane (,,,,,-hexachloro-
cyclohexane) and glyphosate Roundup (-(phosphonomethylamino) acetate)] have
been reported to interfere with StAR protein expression inhibitor Steroidogenesisby
[, ]. The condition lipoid congenital adrenal hyperplasia (lipoid CAH) is
believed to be caused by mutations in the StAR gene. Lipoid CAH is an autosomal
recessive lethal condition in which cholesterol and cholesterol esters accumulate
and a sufficient amount of steroids can not be synthesized by the newly born
child. In humans, StAR knockout mice display a phenotype that is very similar to
lipoid CAH, providing a clear model for studying the mechanism of the important
contribution of StAR protein to steroidogenesis and endocrine production. In
the inner mitochondrial membrane, the cytochrome Pscc side chain cleavage
enzyme, which belongs to the monooxygenase family, transforms cholesterol
to pregnenolone. Three successive monooxygenations are involved in this step:
-hydroxylation, -hydroxylation and C-C bond cleavage. Pregnenolone
then diffuses across the mitochondrial membrane and is translocated to the endo-
plasmic reticulum, where it undergoes a series of testosterone-forming biochemical
reactions. Pregnenolone undergoes C hydroxylation in the Delta  pathway to
form  alpha-hydroxypregnenolone, which is then split between C and C
bonds to form DHEA. The cytochrome P  alpha-hydroxylase/ C,  lyase
catalyzes these reactions []. DHEA could be transformed by the action of β-HSD
to androstenedione and then β-HSD to testosterone. The equilibrium between
these androgens depends on the present activity and type of b-HSD. Types  and
 of b-HSD catalyze the conversion of androstenedione to testosterone and are
expressed in Leydig testis cells, while the opposite reaction occurs in type  (found
among others in prostate and placenta) [].
In steroidogenic and non-steroidogenic tissue such as asthetes, prostate, skin and
brain, the enzymeβ-HSD is commonly expressed. Four β-HSD isozymes exhibit-
ing differential and tissue-specific expression were characterized in the rat. The
spermatic vein transports testosterone into circulation. Testosterone synthesis is
governed by LH in Leydig cells. Testosterone biosynthesis is also regulated by other
factors, such as FSH, insulin-like growth factor- and cytokines []. By paracrine
regulation of testicular functions, FSH also regulates spermatogenesis Figure ).
. Sperm discharge function
The discharge of semen into the reproductive tract of female has to do with the
following steps;
a. Libido: This is the biological need (sexual drive) for sexual activity and is often
expressed as conduct that seeks sex. Its strength is variable over a given time
between people and within an person. In stable older but not younger men,
higher serum testosterone tends to be associated with greater sexual action.
b. Erection: The enlargement and firm state of penis is the erection of the penis.
The dynamic interaction of psychological, neuronal, vascular and endocrine
factors are some of the factors it depends on. When two tubular structures run-
ning the length of the penis, the corpora cavernosa, are engorged with venous
blood, a penile erection occurs. This can result from any of the different physi-
ological stimuli. The corpus spongiosum is a single tubular structure situated
just below the cavernosa corpora, which comprises the urethra from which,
during urination and ejaculation, urine and semen move through. This may
often be slightly engorged with blood, but less so than the penile erection of the
The Concept of Male Reproductive Anatomy
corpora canvernosa normally results from sexual arousal and/or excitement,
but can also occur due to triggers such as a full urinary bladder or spontane-
ously over the course of a day or at night, often during romantic or wet dreams.
Swelling and enlargement of the penis results from an erection. Although it is
not necessary for all sexual activities, erection makes sexual intercourse and
other sexual activities (sexual functions).
c. Ejaculation: Ejaculation and erection must take place for sperm to deliver
into the female genital tract (without technical assistance). Two occurrences
or events should really be considered during ejaculation, the first being
semen deposition into the posterior urethra, called seminal emission, and
the second being semen expulsion from the urethra. The sympathetic nerv-
ous system controls emission and ejaculation of sperm. Emission includes
the intense contraction of the vas, ampulla of the vas, seminal vesicles
and prostate covering muscle and myoid complexes. Ejaculation, along
with contraction of the periurethral muscles, mainly the bulbocavernosus
muscle, requires closure of the bladder neck to avoid or prevent retrograde
semen flow.
d. Orgasm: Organsm, or orgasm, is an intense, pleasurable feeling that typically
happens at the height of sexual arousal, accompanied by a decrease in sexual
tension. Not all sexual arousal results in orgasm, because in order to have an
orgasm, people need various circumstances and different forms and quanti-
ties of stimulation. Orgasm is made up of a rhythmic contraction series. In
the pelvic organs and genital area. Throughout the body, breathing rate, heart
rate, and blood pressure increase dramatically. The general contraction of the
muscles can lead to facial contortions and muscle contractions in the extremi-
ties, back, and buttocks. Organism occurs in two phases in men. First, at the
Figure 6.
Showing the major pathways in steroid biosynthesis.
Male Reproductive Anatomy
base of the urethral, the vas deferens, seminal vesicles, and prostate contract,
sending seminal fluid to the bulb, and the man feels a sense of inevitability of
ejaculation, a sensation that ejaculation is just about to happen or happen and
can not be prevented. Second, a mechanism called ejaculation is closely related
to the urethra bulb and penis rhythmically contracting, expelling the sperm,
but some men experience organism separately from ejaculation.
. Endocrine and neuroendocrine factors regulating testicular
The brain (on stimulation), the master endocrine gland, and local factors gener-
ated by the testes finely regulate the spermatogenic and steroidogenic functions of
the testes. The proliferation of primitive germ cells and the development of the testes
are carefully regulated by testosterone (secreted by the legdig cell on activation by
placenta released human chorionic gonadotropin (HCG)) during intrauterine life
[]. The hormonal control of testes ceases after birth and the testes remain quiet
until the beginning of puberty []. The testicular function setting is triggered at
puberty by certain cells in the hypothalamus that activate GnRH secreting cells
(Figure ). These cells are referred to as kisspeptin secreting cells found in the
periventricular nucleus (PVN), preoptic nucleus (PN) and arcuate nucleus (ARC)
and in the anteroventral perivetricular nucleus (AVPV) [].
Steroids, leptin, and other systemic factors are believed to have effect on the
testicular functions by binding on receptor located on these kisspeptin secreting cells
[]. Kisspeptin stimulates GnRH cells to release gonadotropin releasing hormone
via the median eminence (Figure ). The cells that secrete GnRH are under the regu-
lation of kisspeptin because they express the GPR receptor on their cell membrane
that bind to kisspeptin released by kisspeptin secreting cells. This hormone is carried
to the anterior pituitary through the hypothalmo-hypophyseal portal system.. There
the gonadotropes are stimulated by GnRH to release follicle stimulating hormone
(FSH) and luteinizing hormone (LH) which are the tropics for leydig and sertoli
cells respectively. This is the neuroendocrine axis of testicular regulation. The
gonadotropes in the adenohypophysis, on stimulation, releases LH, FSH and growth
hormone that regulate the functions of the testes. This is the endocrine axis of
Figure 7.
Showing kisspeptin cells connections with GnRH cells (source:
The Concept of Male Reproductive Anatomy
testicular regulation. Spermatozoa development is based on pituitary gonadotropins,
LH and FSH, which are released in response to hypothalamic GnRH pulsatile release.
The testes as an endocrine gland secrete steroid and other local factors that
regulate its function through autocrine and paracrine mechanism. The steroids
and inhibin synthesized by leydig and sertoli cells respectively regulate the neuro-
endocrine and endocrine factors via negative feedback mechanism. Abnormalities
in these levels of testicular regulation results to male reproductive dysfunctions
[, ]. This is hypogonadotropin-hypogonadism due to misdirection in GnRH
cells migration from the olfactory cells during development [].
GnRH act via interacting with a particular receptor found on the cell membrane
of gonadotropes. These receptors are G-protein - coupled receptors that interact
with the hormone to form a hormone receptor complex. This results in the interac-
tion of phosphoinositide with Gp protein hydrolysis and the release of diacylg-
lycerol and inositol triphosphate, resulting in the mobilization of calcium from
intracellular stores and the inflow of extracellular calcium into the cell. The release
of gonadotropin from gonadotropes into the general circulation results from this
calcium influx [].
. Clinical implications of gonadotropins and steroidogenic hormones
LH binds to the receptors located on the Leydig cells in the testis and induces
testosterone synthesis, which in turn could adversely affect the release of hypotha-
lamic and pituitary hormones. FSH targets the receptors on the Sertoli cells and
induces androgen-binding protein production, which helps to transport testosterone
via the Sertoli cells’ tight junction complexes. Sertoli cells are also activated by FSH
to secrete inhibin and activin, both of which have a negative effect on hypothalamus
and pituitary hormone release. The primary endocrine hormone involved in testicular
function control is FSH. FSH has a central role to play in regulating the Sertoli cell
populations, which in turn modulates the number of germ cells proceeding through
the mitotic and meiotic spermatogenesis phases. In mitotic and meiotic spermatogo-
nia, FSH handles or regulate DNA synthesis and also prevents apoptosis induction in
Figure 8.
Regulation of kisspectin-GnRH axis ( It is through this kisspeptin-GnRH axis that factor such
as steroids stress, leptin light and dark etc. influence the functions of the testicles [46].
Male Reproductive Anatomy
Figure 9.
Showing the main product of Leydig cells (e.g testosterone), Regulation, hormonal products, Leydig and
Sertoli cells interaction. AB (androgen binding protein); ATP (adenosine triphosphate); cAMP (cyclic
adenosine monophosphate); E (estradiol); FSH (follicle-stimulating hormone); LH (luteinizing hormone); T
(testosterone) [17].
round spermatids []. It has been shown that FSH stimulates the release of various
products from Sertoli cells. Sertoli cell products have been reported to play a role in
the regulation of the functions of Leydig cells. For successful spermatogenesis and
steroidogenesis, the ability of LH to function on the LH receptors present on Leydig
cells is essential. LH controls the growth of Leydig cells, the number of Leydig cells,
the biosynthesis of testosterone and its secretion. The removal of testosterone has
been shown to induce spermatid detachment from Sertoli cells, resulting in full sper-
matogenesis stoppage. To initiate, sustain, and restore spermatogenesis, testosterone
works synergistically with FSH. In particular, testosterone contributes to the blood-
testis barrier development, the maintenance of interactions between Sertoli and germ
cells, and the release of mature sperm from Sertoli cells). The blood-testis barrier
formation is weakened in the absence of testosterone and germ cells are released from
the Sertoli cells prematurely.
Estrogens, localized in Leydig and Sertoli testis cells, efferent ductules and
epididymis also play a significant role in spermatogenesis control. Evidence suggests
that estrogen is secreted into the seminiferous tubular fluid by germ cells, which
may be essential for the efferent ductules and epididymis functions. It is stated that
estrogen has a stimulatory and inhibitory effect on the proliferation and differentia-
tion of germ cells. It has been shown that administration of aromatase inhibitors
to male monkeys induces decreased spermatogenesis and sperm concentrations,
suggesting estrogen ‘s crucial role in sustaining spermatogenesis. In proliferating
Sertoli cells, high estrogen levels are present and their levels decrease as Sertoli cells
avoid differentiation and start maturation. Estrogens control the expression of the
molecule of cell adhesion, neural cadherins, involved in the maintenance of cell
adhesion of germ cells-Sertoli.
Environmental estrogens is known to have a deleterious effects on male fertil¬ity
and it has been shown that neonatal exposure to exogenous estrogens induces
irreversible alteration of gene expression in the reproductive tract. Testicular
steroidogenesis in adulthood has been shown to impair neonatal sensitivity to
diethylstilbestrol, a synthetic estrogen. Administration of β-estradiol to adult rats
has been shown to induce a decrease in basal and stimulated testosterone production
of – percent. Adult male rats showed a substantial decrease in circulating FSH
The Concept of Male Reproductive Anatomy
and LH concentrations when treated with estradiol, which subsequently contributed
to reductions in serum and testicular testosterone levels. Several other factors, apart
from hormones, have also been shown to affect testicular functions (Figure ).
. Other factors necessary for male reproductive functions
Growth Hormone: This hormone is usually synthesized by the anterior
pituitary (AP) and has effect on virtually all tissues and organs of the body. It
is essential for the general metabolic processes in the testes. It is also necessary
for proliferation of spermatogenesis, and plays a key role in the proliferation,
growth and maturation of spermatids [].
Local Factors: Some of the most important local factors produced in the testes
by the leydig cells are testosterone and insulin-like factor while that of sertolin
cells of thae testes are inhibin, growth factor. Stem cell factors, immunological
factors, opioids, oxytocin, vasopressin, peritubular cell modifying factors,
rennin, angiotensin, GnRH, CRH, ACTH, GHRH, calmudilin, pasminogen
activator, metalloproteases, dinophin, PACAP etc. are some of the other local
factors that are believed to have effects on the functions of the testes [].
Apart from these factors, glucose has also been shown to be important for
proper functioning of testis.
Insulin signaling and glucose transport: Apart from these factors, glucose
has also been shown to be important for proper functioning of testis. Glucose
is very critical for high-energy, challenging testicular spermatogenesis and ste-
roidogenesis to be successfully accomplished. It has been shown that cytocha-
lasin B, a glucose transport inhibitor, competitively binds to proteins that are
involved in Leydig cells’ facilitated glucose absorption, and inhibits testoster-
one synthesis stimulated by LH. In the presence of glucose, high testosterone
production has been observed, suggesting the need of this compound for tes-
tosterone production in addition to LH, and it has also been shown that there is
no testosterone production in the absence of glucose. The family of facilitative
glucose transporter (GLUT) proteins carries out glucose transfer through
the plasma membranes. There are  GLUT protein families that have been
identified to date. Glucose transporter- to  expressions in different types
of rat testicular cells has been demonstrated. Mature spermatozoa also express
glucose transporters because they require glucose for basic cell activity as well
as for specific functions such as motility and fertilizing capacity []. One
of the recently cloned members of the GLUT family, GLUT- is known to be
the leading transporter of glucose in the testis. In the heart, skeletal muscles,
brain, spleen, prostate and intestine, GLUT- is expressed, but its expression
was found to be highest in the testis relative to all other tissues [, ], thus
indicating the involvement of GLUT  in glucose transport for steroidogenesis
of Leydig cells []. In addition, in testicular cell types, GLUT- has also
been shown to be abundantly expressed. The high expression in the testis of
insulin signaling molecules and glucose transporters suggests the high energy
expenditure of contractile testicular cells and the dependency on glucose as an
energy source. The insulin receptor family also plays an important role in the
development of gonads in the testis. The differentiation of the testis is caused
by the sex-determining region Y (SRY) expression present in somatic progeni-
tor cells intended to become Sertoli cells. Sertoli, Leydig, interstitial and myoid
cells have been shown to express IRS- and IRS-, suggesting the reliance of
Male Reproductive Anatomy
Author details
Oyovwi MegaObukohwo*, Nwangwa EzeKingsley, Rotu ArientareRume and
 Department of Hunan Physiology, Achievers University, Owo,OndoState, Nigeria
 Faculty of Basic Medical Science, Department of Physiology, Delta State
University, Abraka, Nigeria
 Department of Physiology, University of Ibadan, Ibadan,OyoState, Nigeria
 Department of Physiology, University of Medical Sciences, Ondo,OndoState,
*Address all correspondence to:
these cell types on insulin. Sperm motility, progressive motility and acrosome
reaction of human spermatozoa have been reported to increase by insulin
and leptin, thereby improving their fertilizing ability. In addition, it has been
shown that human spermatozoa releases pulsatile insulin, which is autocrine-
regulated, and it has been hypothesized that insulin derived from sperm can
play a role in sperm capacitation []. Therefore, insulin plays an important
role in the proper functioning of the testis and in preserving the capacity of
spermatozoa to fertilize. Insulin signaling and glucose transport in the body
are known to be affected by many factors. Of the different variables, as one of
the main regulators of glucose homeostasis in the body, reactive oxygen species
(ROS) are involved. While low ROS levels are important for the signaling of
insulin, increased ROS could have a negative impact on homeostasis of glucose.
©  The Author(s). Licensee IntechOpen. This chapter is distributed under the terms
of the Creative Commons Attribution License (
by/.), which permits unrestricted use, distribution, and reproduction in any medium,
provided the original work is properly cited.
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This study explored the effects of Cocos nucifera L. water (CW) on the hypothalamo-pituitary-gonadal axis (HPG) and fertility in Wistar rats. Adult male and female Wistar rats were treated orally as follows; Study 1: Group 1: control (distilled water), group 2: 20 ml/kg corn oil (danazol vehicle), group 3: 20 ml/kg CW, group 4: 40 ml/kg CW, group 5: danazol, group 6: danazol + 20 ml/kg CW and group 7: danazol + 40 ml/kg CW. 200 mg/ kg danazol was administered. Serum levels of LH, FSH, estradiol and testosterone; gonadal weights and sperm indices were assessed. Study 2: Group 1: control (distilled water), group 2: 20 ml/kg CW, group 3: 40 ml/kg CW for 6 and 2 weeks prior to mating in male and female rats respectively. Significant (p < 0.05) increases in estradiol concentration were observed in groups 3, 4, 6 and 7. Significant reductions in LH, FSH, estradiol and testosterone levels were observed in group 5 which were ameliorated in groups 6 and 7. Males showed significant increases in sperm count and motility in groups 3, 4, 6 and 7, and reductions in these variables along with viability in group 5. CW pre-treatment increased fecundity index and proportion of female pups from dams, while the pups from sires showed higher birth weights. CW acts on the HPG to positively influence reproductive function in both males and females and may aid in maternal preconception sex selection of female offspring.
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The germ cell development strategy during spermatogenesis was investigated in the black swamp snake (Seminatrix pygaea). Testicular tissues were collected, embedded in plastic, sectioned by ultramicrotome, and stained with methylene blue and basic fuchsin. Black swamp snakes have a postnuptial pattern of development, where spermatogenesis occurs from May to July and spermiation is completed by October. Though spatial relationships are seen between germ cells within the seminiferous epithelium during specific months, accumulation of spermatogonia and spermatocytes early in spermatogenesis and the depletion of spermatocytes and accumulation of spermatids late in spermatogenesis prevent consistent cellular associations. This temporal germ cell development within an amniotic testis is consistent with that seen in other recently studied temperate reptiles (slider turtle and wall lizard). These reptiles’ temporal development is more similar to the developmental strategy found in anamniotes than the spatial germ cell development that characterizes birds and mammals. Our findings also imply that a third germ cell development strategy may exist in temperate breeding reptiles. Because of the phylogenetic position of reptiles between anamniotes and other terrestrial amniotes, this common germ cell development strategy shared by temperate reptiles representing different orders may have significant implications as far as the evolution of sperm development within vertebrates.
Basal and LH/human chorionic gonadotropin (hCG)stimulated testosterone formation by Leydig cells is dependent on ambient glucose levels. Inhibition of glucose uptake is associated with decreased testosterone formation. Recently, glucose transporter 8 (GLUT8) has been shown to be highly expressed in the testis. In the present study, we have investigated the expression and regulation of the GLUT8 gene in rat Leydig cells. Primers were designed by using sequences that are not conserved in GLUT1 to GLUT5 and that contain the glycosylation region of GLUT8. This yielded an amplicon of 186 bp. The tissue-specific expression experiments in adult rat (55- to 65-day-old) tissues revealed that GLUT8 is expressed predominantly in the testis, in smaller amounts in heart and kidney, and in negligible amounts in liver and spleen. Furthermore, GLUT8 mRNA was found to be highly expressed in crude interstitial cells, Leydig cells and testicular and epididymal germ cells. In prepubertal rat (20-day-old) tissues, GLUT8 expression was comparatively much lower than in the adult rat tissues. By comparative RT-PCR, hCG caused dose- and timedependent increases of GLUT8 mRNA levels. hCG and IGF-I had synergistic effects on GLUT8 mRNA and protein expression. GLUT1 and GLUT3 were also found to be expressed in Leydig cells. However, neither GLUT1 nor GLUT3 were affected by treatments with hCG, IGF-I or hCG and IGF-I combined. The addition of murine interleukin-1 (mIL-1; 10 ng/ml), murine tumor necrosis factor- (mTNF-; 10 ng/ml), murine interferon(mIFN-; 500 U/ml) separately or in combination decreased hCG-induced GLUT8 mRNA levels significantly. In conclusion, GLUT8 mRNA in Leydig cells was positively regulated by hCG and IGF-I and downregulated by cytokines, mIL-1, mTNF- and mIFN-. These results indicate that hCG, growth factors and cytokines affect Leydig cell steroidogenesis by modulating GLUT8 expression.
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