A1,
A2,
B,
C1,
C2,
D,
E,
F,
G-H,
I-K,
L,
M,
N,
O,
P1,
P2,
Q-R,
S,
T,
U-V,
W-Z
Delatestryl Pharmacology, Pharmacokinetics, Studies, Metabolism - Testosterone Enanthate
Delatestryl Pharmacology, Pharmacokinetics, Studies, Metabolism - Testosterone Enanthate
CLINICAL PHARMACOLOGY
Endogenous androgens are responsible for the normal
growth and development
of the male sex
organs and for maintenance of secondary
sex characteristics. These
effects include growth
and maturation of
prostate, seminal
vesicles, penis, and scrotum; development
of male hair
distribution, such as beard,
pubic, chest, and axillary
hair; laryngeal enlargement;
vocal chord thickening;
alterations in body musculature;
and fat distribution.
Androgens also cause
retention of nitrogen,
sodium, potassium,
and phosphorus, and decreased urinary
excretion of calcium.
Androgens have been reported to increase protein
anabolism and decrease
protein catabolism.
Nitrogen balance is improved only when there is sufficient intake
of calories and protein.
Androgens are responsible for the growth
spurt of adolescence
and for the eventual termination
of linear growth
which is brought about by fusion of the epiphyseal growth
centers. In children, exogenous
androgens accelerate linear growth
rates but may cause a
disproportionate advancement
in bone maturation. Use over long periods may result in fusion
of the epiphyseal growth centers and termination
of growth process. Androgens
have been reported to stimulate
the production of
red blood
cells by enhancing the production of erythropoietic stimulating
factor.
During exogenous
administration
of androgens, endogenous
testosterone release is inhibited through feedback
inhibition of pituitary
luteinizing hormone (LH). At
large doses of exogenous
androgens, spermatogenesis
may also be suppressed through feedback
inhibition of pituitary
follicle stimulating
hormone (FSH).
There is a lack of substantial evidence
that androgens are effective in fractures, surgery,
convalescence, and functional
uterine bleeding.
Pharmacokinetics
Testosterone esters are less polar
than free testosterone. Testosterone esters in oil
injected intramuscularly
are absorbed slowly from the lipid phase; thus testosterone
enanthate can be given at intervals of two to four weeks.
Testosterone in plasma
is 98 percent bound
to a specific testosterone-
estradiol binding globulin, and about two percent
is free. Generally, the amount of this sex- hormone
binding globulin in
the plasma will
determine the distribution
of testosterone
between free and bound
forms, and the free testosterone
concentration
will determine its half-life.
About 90 percent of
a dose of testosterone
is excreted in the urine as glucuronic and sulfuric acid
conjugates of testosterone
and its metabolites; about six percent
of a dose is excreted in
the feces, mostly in the unconjugated form. Inactivation of testosterone
occurs primarily in the liver. Testosterone is metabolized to various
17-keto steroids through two different pathways. There are considerable
variations of the half- life
of testosterone
as reported in the literature, ranging from 10 to 100 minutes.
In responsive tissues, the activity
of testosterone
appears to depend on reduction
to dihydrotestosterone, which binds to cytosol
receptor proteins.
The steroid-receptor complex
is transported to the nucleus
where it initiates transcription events and cellular
changes related to androgen
action.
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