Spermatogenesis and Spermiogenesis
Spermatogenesis refers to the entire process of converting the original
diploid precursor of spermatozoa (bearing 46 chromosomes), the spermatogonia
into haploid spermatozoa 9bearing 23 chromosomes). The spermatogenic cycle from
spermatoonia to spermatozoa starts at puberty and last about 9 weeks. This
process is initiated by testosterone secreted by Leydig cells. Under the
influence of testosterone, spermatogonia proliferate rapidly by mitotic
division to produce primary spermatocyte. Primary spermatocyte enters meiosis I
or the first meiotic division and produces a secondary spermatocyte. The secondary spermatocytes undergo
meiosis II and form haploid spermatids (23 chromosomes). The spermatid
being haploid can be used for in vitro fertilization since it has acquired the
status of a mature spermatozoon.
How a spermatids develops into spermatozoa?? . Formation of spermatozoa
involves three events and this is known as spermiogenesis.
1.
Acrosome formation: The acrosomal
granule is made of coalition of Golgi membranes and the granules wrap round the
nucleus to form and acrosomal cap.
2.
The tail and midpiece formation of
the spermatozoon is formed by the movement of the centriole towards the tail
end of the acrosomal ends. Centriole
forms the flagellum. Mitochondria group around the junction of the tail and the
head forming the midpiece. The matured spermatozoon now has a nuclear
condensation in the head. The residual tissues remaining after formation of
spermatozoa is engulfed by Sertoli cell.
Hormonal requirement of spermatogenesis:- Normal spermatogenesis requires
action of both pituitary gonadotropins –
LH and FSH. This is the rule at least at the onset of puberty. LH stimulates
Leydig cells, which produce testosterone. FSH initiates function function in
immature Sertoli cells even before the beginning of spermatogenesis. This helps
in producing a blood/testis barrier and secretion of tubular fluid and other
products required for spermatogenesis. Once spermatogenesis is established,
Sertoli cells function independent of FSH. In view of this, the contributions
made by the two gonadotropins in maintaining spermatogenesis in adults are
probably superfluous. Normal
spermatogenesis is totally dependent on the local source of testosterone
produced by the Leydig cells of the testis. The concentration of testosterone
in testis is at least 25 to 50 times responsible for testosterone production,
in hypogonadotrophic population may fall. But in men with hypogonadotrophism,
medical treatment consists of giving both LH and FSH to enhance
spermatogenesis. FSH alone is ineffective without testosterone and for
production of testosterone LH(hCG) is necessary. FSH is said to maintain
spermatogenesis. in a quantitative fashion by increasing spermatogoneal mitosis
while testosterone is essential for steps in meiosis and spermiogenesis. So
testosterone and FSH act synergistically if administered in pharmacological
doses. Reactive Oxygen Species (ROS) in males : The role played by drugs to
counterattack the cellular damage in sperms ??
Free oxygen redicals cause peroxidative damage to sperm plasma membrane.
These are released by degenerating, dying tissues in culture media. Seminal
plasma contains ROS in considerable quantity. Human spermatozoa seem to require
ROS for some of their physiological processes like hyperactivated motility and
acrosome reaction. But, at the time of fertilization in in vitro condition,
excessive exposure of ROS can cause DNA damage both to spermatozoa and to
oocyte and also embryonic cell membrane. Antioxidants like Vit E, Vit C,
taurine, hypotaurine and glutathione can give protection to these membranes
against oxidative DNA damage. Leukocytes present in the semen can add to the
quantity of ROS produced in the culture.
The mother of immature sperms when sperms were in infancy!! Who looked after those would be sperms??
Sertoli cells are mother cells, which feed the primitive stem cells starting
from the level of spermatogonia. The cut section of seminiferous tubule shows
the periphery of the tubule formed peritubular myoid cells. Resting on the
inner lining of the myoid cells, there are sertoli cells (SC) connected to each
other by tight junction. The SC extends from the basement membrane to the
lumens. At the level of the basement membrane they from tight junctions with
one another, thus dividing the tubular epithelium into a basal outer
compartment, which has a functional permeability barrier with no contact with
systemic circulation. So, the spermatogonia and their further development into
spermiogenesis occur in the avascular microenvironment. The metabolic support
for these developing germ cells is given entirely by Sertoli cells. Sertoli
cells possess receptor for FSH in their plasma membrane and receptors for
androgens in their nuclei.
The functions of the Sertoli
cells are:
1.
To sustain the germ cells. They
metabolize glucose into lactate and pyravate and synthesize transferring
necessary for iron delivery to the germ cells.
2.
Each Sertoli cell is in contact with
about 47 germ cells to which they give physical support.
3.
Sertoli cells produce specific
proteins such as androgen binding proteins (ABP) and inhibin.
4.
They maintain a blood testis barrier
along with the ovoid cells and make a physical support for the germ cells. If
the barrier
Is broken ,e,g. by infection or scrotal injury the inflammatory cells of
the body get access to the germ cells and this can give room to formation of
antisperm antibodies.
5.
Sertoli cells form the principle site
for receiving the follicle-stimulating hormone(FSH). ABP is synthesized and
secreted into seminiferous tubules by Sertoli cells. The secretion of ABP binds
the intratesticular androgens, which are retained in the testis for the purpose
of spermatogenesis. ABP is very similar to sex hormone binding globulin (SHBG)
produced in the liver. The difference between SHBG and ABP is mainly in the
carbohydrate content.
Sertoli Cell Only Syndrome
This syndrome is seen in conditions where the testicular tissue has been
destroyed by disease with the result, seminiferous tubules do not have any germ
cell production. This condition is also known as maturation arrest; when a
testicular biopsy is done in this condition most of the tubules show only
Sertoli cells and it is assumed that this kind of patients cannot be taken up
for ICSI through TESE. But it has been found that the testicular atrophy is not
total. In about 50 percent of cases, a careful search through the testis can show
at least a few tubules showing spermatogenesis.
Sperm Transport in Male and Female Reproductive Tract
The spermatozoa complete the journey from seminiferous tubule to external
urethral meatus while doing so the spermatozoa mature along the genital tract
and develop capacitation and activation in the female genital tract. On
entering the epididymis from vasa efferentia, the composition and volume of
semen changes. The spermatozoa get concentrated by fluid absorption from 50
million/ml on entry to same 5000 million/ml while leaving the epididymis.
Epididymis adds secretory products like carnitine and glycerol phosphoryl
choline and changes the glycoprotein profile on the surface of the
spermatozoon.
Semen is deposited in the
post vaginal fornix during sexual intercourse. The spermatozoa penetrate
rapidly into cervical mucus (CM). The CM is scanty and viscous during most of
the menstrual cycle but the character changes completely during the period of
ovulation becoming copious and thinner. The mucus is secreted by the secretory
cells in endocervical canal (see ervical mucus C). The physical characters of
mucus change in order to bar the entry of spermatozoa during the non-ovulatory
period, thus limiting its entry in the mid-cycle only so that the sperm are able
to gain access to the ovum awaiting in the fimbrial portion of the tube. The
spermatozoa display linear migration for a short period of 1 to 2 days in the
mid-cycle. The beating of the sperm flagellum is greater in the ovulatory
cervical mucus that either in seminal plasma or any of the culture fluids. The
maximum score (Insler Score 12) of cervical mucus improves with estrogen peak,
thus demonstrating the fact that the cervical glands are dependent on changing
levels of estrogen. Cervical canal has crypts or glands, which produce cervical
mucus that contains glucose and other source of energy. It forms a reservoir of
spermatozoa inside the glands. The CM also removes inactive spermatozoa.
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