spermatogenesis Reeshma.PPT

spermatogenesis Reeshma

1. Spermatogenesis

2. Spermatogenesisis the process by which
male germ cell (spermatogonia) develop into
mature spermatozoa.
Spermatozoa are the mature male gametes in
many sexually reproducing organisms.
Thus, spermatogenesis is the male version of
gametogenesis.
In humans it takes on an average 74 days to
form a mature sperm

3. It starts at puberty and usually continues
uninterrupted until death, although a
slight decrease can be discerned in the
quantity of produced sperm with increase
in age.
The entire process can be broken up into
several distinct stages, each
corresponding to a particular type of cell:

5. The initial stages occur within the testes and progress
to the epididymis where the developing gametes
mature and are stored until ejaculation.
The seminiferous tubules of the testes are the starting
point for the process, where stem cells adjacent to the
inner tubule wall divide in a centripetal direction.
The cells begin to divide at the walls proceeding
towards the lumento produce immature sperm.
Maturation occurs in the epididymis and involves the
acquisition of a tail and hence motility.

6. Stages of Spermatogenesis
A diploid spermatogoniumwhich resides in
the basal compartment of seminiferous
tubules, divides mitotically to produce two
diploid intermediate cell called a primary
spermatocyte.
Each primary spermatocyte then moves into
the adluminal compartment of the
seminiferous tubules and duplicates its DNA
and subsequently undergoes meiosisto
produce two haploid secondary
spermatocytes.

7. Secondary spermatocytes undergo a second
meiotic division to form spermatidswith
haploid no of chromosomes.
Spermatids mature to form the Sperm/
spermatozoa and this process is termed
spermiogenesis.
During spermiogenesis, the spermatids begin
to grow a tail, and develop a thickened mid-
piece, where the mitochondria gather.

8. Spermatid DNA also undergoes packaging,
becoming highly condensed.
The DNA is packaged firstly with specific
nuclear basic proteins, which are subsequently
replaced with protamines during spermatid
elongation.
Maturation then takes place under the
influence of testosterone, which removes the
remaining unnecessary cytoplasm and
organelles

9. The excess cytoplasm, known as residual
bodies, is phagocytosed by surrounding Sertoli
cells in the testes.
The resulting spermatozoa are now mature but
lack motility, rendering them sterile.
The mature spermatozoa are released from
the protective Sertoli cells into the lumen of the
seminiferous tubule in a process called
spermiation.

10. Structure of a mature sperm

11. A mature spermatozoa, or spermatozoon, has
3 distinct parts: a head, a mid-piece, and a tail.
The head contains 23 chromosomes within a
nucleus.
The tip of the nucleus is covered by a cap
called the acrosome, which contain enzymes
needed to breach the egg for fertilization.
The mid-piece contains energy-producing
mitochondria.
The tail is made up of microtubules that form
cilia and flagella.

12. It should also be noted that not all
spermatogonia divide to produce
spermatocytes, otherwise the supply
would run out.
Instead, certain types of spermatogonia
divide to produce copies of themselves,
thereby ensuring a constant supply of
gametogonia to fuel spermatogenesis.

13. A normal human male usually produces
several hundred million sperm per day.
The estimated number of spermatids
formed from a single spermatogonium is
estimated to be 512.
Sperm are continually produced
throughout a male's reproductive life,
though production decreases with age.

14. The non-motile spermatozoa are transported
to the epididymis in testicular fluidsecreted by
the Sertoli cells with the aid of peristaltic
contraction.
Whilst in the epididymis they acquire motility
and become capable of fertilisation.
However, transport of the mature spermatozoa
through the remainder of the male
reproductive system is achieved via muscle
contraction rather than the spermatozoon's
recently acquired motility.

15. During ejaculation, sperm leaves the
penis in a fluid called seminal fluid
(semen).
This fluid is produced by 3 types of
glands, the seminal vesicles, the
prostate gland, and Bulbourethral gland
(Cowper's glands).
Each component of a seminal fluid has a
particular function.

16. Sperm are more viable in a basic solution, so
seminal fluid has a slightly basic pH balance.
Seminal fluid also acts as an energy source for
the sperm, and contains chemicals that cause
the uterus to contract.
An average volume per ejaculate is 2.5-3.5 ml
Normal sperm count is100 million
sperms/ml

17. Role of Sertoli cells
Sertoli cells serve a number of functions
during spermatogenesis, they support
the developing gametes in the following
ways:
Maintain the environment necessary for
development and maturation via the
blood-testis barrier
Secrete substances initiating meiosis
Secrete supporting testicular fluid

18. Secrete androgen-binding protein, which
concentrates testosterone in close
proximity to the developing gametes
Secrete hormones effecting pituitary
gland control of spermatogenesis,
particularly the polypeptide hormone,
inhibin
Inhibin decreases FSH secretion.
Phagocytise residual cytoplasm left over
from spermiogenesis

19. Factors influencing
spermatogenesis
The process of spermatogenesis is highly
sensitive to fluctuations in the environment,
particularly hormones and temperature.
Testosterone is required in large local
concentrations to maintain the process, which
is achieved via the binding of testosterone by
androgen binding protein present in the
seminiferous tubules.
Testosterone is produced by Leydig cells,
which reside adjacent to the seminiferous
tubules.

20. Seminiferous epithelium is sensitive to
elevated temperature in humans and
spermatogenesis will be adversely affected by
temperatures as high as normal body
temperature.
Consequently, the testes are located outside
the body in a sack of skin called the scrotum.
The testes are kept cool at a temp. of about
32°C by;
Air circulating around the scrotum
Heat exchange in a counter current fashion
between the spermatic arteries and veins

21. Other factors influencing
spermatogenesis
Dietary deficiencies (such as vitamins B, E
and A)
Anabolic steroids
Metals (cadmium and lead)
x-ray exposure
Drugs like digoxin
Alcohol and
Infectious diseases will also adversely affect
the rate of spermatogenesis.

22. Composition of human semen
Color: white, opalescent
Sp gravity: 1.028
pH: 7.35-7.5
Average sperm count: 100 million/ml
Components:
Fructose
Prostaglandins

23. Ascorbic acid
Phosphorylcholine
Flavins
Cholesterol
Phospholipids
Fibrinolysin
Phosphate and bicarbonate buffers etc.

24. Hormonal control
Hormonal control of spermatogenesis varies
among species.
In humans the mechanism are not completely
understood, however it is known that initiation
of spermatogenesis occurs at puberty due to
the interaction of the hypothalamus, pituitary
gland and Leydig cells.
If the pituitary gland is removed,
spermatogenesis can still be initiated by follicle
stimulating hormone and testosterone.

25. During puberty the hypothalamus
releases gonadotropin-releasing
hormone (GnRH).
The anterior pituitary produces the
gonadotropins; follicle-stimulating
hormone (FSH) and luteinizing hormone
(LH).

26. Follicle stimulating hormone stimulates
both the production of androgen binding
protein by Sertoli cells, and the formation
of the blood-testis barrier.
FSH stimulates secretion of Inhibin
which has a negative feed back on FSH
secretion.
FSH may initiate the sequestering of
testosterone in the testes, but once
developed only testosterone is required
to maintain spermatogenesis.

27. Luteinizing Hormone
In both sexes, LH stimulates secretion of
sex steroids from the gonads.
In the testes, LH binds to receptors on
Leydig cells, stimulating synthesis and
secretion of testosterone.
Testosterone in turn inhibits LH secretion

28. Regulation of secretion

29. Endocrine function of testes
(Testosterone)
Like other steroid hormones,
testosterone is derived from cholesterol.
The largest amounts of testosterone are
produced by the testes in men.
It is also synthesized in far smaller
quantities in women by the thecal cells of
the ovaries, by the placenta, as well as
by the zona reticularis of the adrenal
cortex in both sexes.

30. Like most hormones, testosterone is
supplied to target tissues in the blood
where much of it is transported bound to
a specific plasma protein (sex steroid
binding globulin).

31. Functions of testosterone
In general, androgens promote protein
synthesis and growth of those tissues
with androgen receptors.
In addition to their action during
development, it exerts an inhibitory
feedback effect on pituitary LH secretion.
It maintains spermatogenesis

32. Testosterone effects can be classified as
virilizing and anabolic, although the
distinction is somewhat artificial, as
many of the effects can be considered
both.

33. Anabolic effectsinclude,
Growth of muscle mass and strength,
Increased bone density,
Stimulation of linear growth and
Bone maturation.

34. Virilizing effectsinclude;
Maturation of the sex organs, particularly
the penis and the formation of the
scrotum in unborn children.
And after birth (usually at puberty) a
deepening of the voice, growth of the
beard and axillary hair.
Many of these fall into the category of
male secondary sex characteristics.

35. Secondary sex characteristics in
Male
Growth of body hair, including underarm,
abdominal, chest, and pubic hair
Greater mass of thigh muscles
Growth of facial hair
Enlargement of larynx and deepening of voice
Increased stature; adult males taller than adult
females, on average
Heavier skull and bone structure

36. Increased muscle mass and strength
Broadening of shoulders and chest;
shoulders wider than hips
Increased secretions of oil and sweat
glands, often causing acne and body odor
Coarsening or rigidity of skin texture, due to
less subcutaneous fat
A prominent Adam's apple

37. Fat deposits mainly around the abdomen
and waist
Higher waist to hip ratio than prepubescent
or adult females or prepubescent males, on
average
On average, larger hands and feet than
prepubescent or adult females or
prepubescent males

38. Mechanism of action of
Testosterone
Free testosterone (T) is transported into the
cytoplasm of target tissue cells, where it can
bind to the androgen receptor, or can be
reduced to 5α-dihydrotestosterone (DHT) by
the cytoplasmic enzyme 5-alpha reductase.
DHT is more potent than T.
DHT binds to the same androgen receptor
even more strongly than T, so that its
androgenic potency is about 2.5 times that of
Testosterone.

39. The T-receptor or DHT-receptor complex
undergoes a structural change that
allows it to move into the cell nucleus
and bind directly to specific nucleotide
sequences of the chromosomal DNA.
This influence transcriptional activity of
certain genes, producing the androgen
effects.

40. T-receptor complexes are responsible for the
maturation of wolffian duct structures and
consequently for the formation of male internal
organ during development.
DHT-receptor complexes are needed to form
the external genitalia in males
Note: if there is a 5-alpha reductase
deficiency, the male body will continuegrowing
into a female with testicles, condition called
pseudohermaphroditism.

41. Male pseudohermaphroditism
Individuals with this syndrome are born
with male internal genitalia with testes,
but have female external genitalia.
They are usually raised up like girls.
However, when they reach puberty, there
is LH secretion and the levels of
circulating testosterone increases.
Consequently they develop male body
contours.

42. Abnormalities of testicular function
CRYPTORCHIDISM: (undescended testes)
In this condition, after the formation of testes in
the abdomen, their descent is incomplete.
Chances of malignancy is high in
undescended testes than the scrotal testes.
This is because, after puberty the high
temperatures cause irreversible damage to the
spermatogenic epithelium.
Treatment is administration of gonadotropic
hormone in early childhood or surgical
correction

43. Male hypogonadism
The clinical picture depends upon
weather the testicular deficiency
develops before or after puberty.
In adults, if it is due to testicular disease,
circulating gonadotropin levels are
elevated-hypergonadotropic
hypogonadism

44. If the defect lies in the hypothalamus or
pituitary, circulating gonadotropin levels
are low-hypogonadotropic
hypogonadoism.
When the endocrine function of testes is
lost in adulthood, the secondary sex
characteristics regress gradually but the
voice remains deep as the laryngeal
growth is permanent.

45. When the Leydig cell deficiency starts from
childhood, the clinical picture is like that of
Eunuchodism.
Characteristic features are;
Individuals above 20yrs are tall (not as in
Gigantism) as their epiphysis remains open
and growth continues post puberty.
Narrow shoulders
Small muscles

46. Small genitalia
Voice high pitched
Pubic and axillary hair present due to
androgens from adrenal cortex but of the
female pattern