Men Contraception Flashcards
Spermatogenesis (stem cell to mature spermatozoa)
64days
LH receptors are one
Leydig cell (steroidogenic cell in testis)
End result of LH and FSH is
increase in steroidogenic capacity/activity of cells in the testis
Leydig cell role
produce testosterone
Sertoli cells role
help the germ cells to communicate and assist the development of germ cells into spermatozoa.
Sertoli cells
Leydig cells
intra or extracellular?
S: intracellular (inside seminiferous tubule)
L: extracellular (outside, between the seminiferous tubules)
Daily production of testosterone
5-7mg
LG receptors are what type of receptor?
G-protein coupled receptors (cAMP activate kinase –> INCREASE AVAILABILITY OF CHOLESTEROL)
Testosterone is converted into:
by the enzyme:
Dihydrotestosterone (DHT)
5alpha-reductase
Some male caracteristics attribute to the androgen exposure are due to
Dyhydrotestosterone (DHT) NOT TESTOSTERONE
Most potent of the steroid?
Estrogens
Testosterone can be converted to
Dihydrotestosterone (DHT) and Estrogens
If give aromatase blockers to male, what happen?
(inhibite estrogens synthesis) Sexe drive decrease in male bc estrogen play important role in sex drive!
DHT and testosterone bing to
androgen receptor
Androgen structure
DNA binding domain, N-terminal domain and a ligand-binding domain.
DNA-binding domain or the androgen receptor interact with
specific Androgen response element (ARE) in the genome.
If we give increase sustained doses of testo, we will observe in the level of testosterone:
we will observe on the spermatogenesis?
Level remain constant du to - feedback, but we reach a point after where sudden spike/spurt of testosterone.
We still have endogenous testosterone, no turning off.
After, in middle, shut down by - feedback. No more production of testo. As the level of exogenous testo give,, spermatogenesis turn back ON.
To effectively turn OFF spermatogenesis/shutdown the HPG axis we should give
a mixture of testo and estradiol (more potent!)
When administrating testo-estradiol what do we observe?
NO change in seminal vesicle weight, serum testosterone, in the others physiological responses, level of androgen.
How chemicals can affect spermatogenesis?
Killing mitotic cells
What happen if we block or deprived the activation of retinoid acid?
No more spermatogenesis bc need retinoid acid.
Non-hormonal suppression of sperm production:
Gossypol (found in cotton sedd oil extract)
Testosterone is useful for
ONLY androgen deficiency!
Consequences of excess androgen use:
Gonadotropin suppression
Sterility
increase LDL & decrease HDL (Atherogenesis)
Support growth of seminal vesicles weight & of prostate (can lead to prostate diseases)
Side effect of excess androgen use:
Headaches, baldness, impotence, aggressive behavior, shrinkage of testicles, development of breast.
Communication of the Leydig and sertoli cells with the germ cells is by:
Paracrine