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Showing posts with label Ethylestrenol (Maxibolin. Show all posts
Showing posts with label Ethylestrenol (Maxibolin. Show all posts

Plasma fibrinolytic activity following oral anabolic steroid therapy.

. Monday, 14 July 2008
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Thromb Diath Haemorrh. 1975 Sep 30;34(1):236-45.

Plasma fibrinolytic activity following oral anabolic steroid therapy.

Walker ID, Davidson JF, Young P, Conkie JA.

Six anabolic steroids were assessed for their ability to enhance plasma
fibrinolytic activity in males with ischaemic heart disease. Five
17alpha-alkylated steroids (Ethyloestrenol, Norethandrolone, Methandienone,
Methylandrostenediol and Oxymetholone) were examined and all produced a
significant increase in plasma plasminogen activator as measured by the
euglobulin lysis time. The only non-17alpha-alkylated steroid studied
(Methenolone acetate) failed to enhance fibrinolysis. The 17alpha-alkylated
steroids studied all deserve more detailed evaluation of their long term effects
on plasma fibrinolytic activity.

Induction of premature menstruation with anabolic steroids.

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Am J Obstet Gynecol. 1973 Sep 1;117(1):121-5.

Induction of premature menstruation with anabolic steroids.

Bolch OH Jr, Warren JC.

PIP: To determine the mechanism of the effect of certain anabolic steroids on
menstruation induction and to evaluate this effect as an interceptor of early
pregnancy, the luteal phase length was studied in the cycles of women ranging in
age from 21 to 37 years after postovulatory treatment with 7 different anabolic
steroids. Basal body temperature records were kept and endometrial biopsies were
obtained late in the pretreatment control periods to confirm ovulation. 2
steroids which had been proven to shorten the luteal cycle phase were
administered as follows: Nandrolone phenpropionate was given in a daily 50-mg
dose intramuscularly for 3 days. 30 mg of oxymetholone was administered orally
every 6 hours for 4 days. The previously untested steroids were administered
orally in evenly divided doses every 6 hours for 4 days as follows: oxandrolone,
60 mg daily; stanozolol, 28 mg; methandrostenolone, 60 mg; fluoxymesterone, 40
mg; and ethylestrenol, 30 mg. Plasma progesterone and gonadotropins were measured
by radioimmunoassay of blood samples taken 7 days after ovulation. Nandrolone and
oxymetholone were found to significantly shorten cycle and luteal phase lengths
and depress plasma LH and progesterone levels as compared to control cycles.
Nandrolone also significantly depressed plasma FSH levels. Of the 5 new drugs,
only ethylestrenol significantly shortened luteal phase length (p less than
.001). This finding is questioned by the small sample size and thus the use of
this steroid as a menstruation inducer is considered questionable. The mechanism
of the effect of nandrolone and oxymetholone appears to be due to their
antigonadotropic action that only secondarily reduces progesterone levels.
Whether these steroids can affect human chorionic gonadotropin and thus cripple
the corpus luteum and interrupt early pregnancy needs further research.

Relative binding affinity of anabolic-androgenic steroids: comparison of the binding to the androgen receptors in skeletal muscle and in prostate, as well as to sex hormone-binding globulin.

. Wednesday, 2 July 2008
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Saartok T, Dahlberg E, Gustafsson JA.

Relative binding affinity of anabolic-androgenic steroids: comparison of the binding to the androgen receptors in skeletal muscle and in prostate, as well as to sex hormone-binding globulin.

Endocrinology. 1984 Jun;114(6):2100-6.

ABSTRACT: It is unclear whether anabolic steroids act on skeletal muscle via the androgen receptor (AR) in this tissue, or whether there is a separate anabolic receptor. When several anabolic steroids were tested as competitors for the binding of [3H]methyltrienolone (MT; 17 beta-hydroxy-17 alpha-methyl-4,9,11-estratrien-3-one) to the AR in rat and rabbit skeletal muscle and rat prostate, respectively, MT itself was the most efficient competitor. 1 alpha-Methyl-5 alpha-dihydrotestosterone (1 alpha-methyl-DHT; mesterolone) bound most avidly to sex hormone-binding globulin (SHBG) [relative binding affinity (RBA) about 4 times that of DHT]. Some anabolic-androgenic steroids bound strongly to the AR in skeletal muscle and prostate [ RBAs relative to that of MT: MT greater than 19-nortestosterone ( NorT ; nandrolone) greater than methenolone (17 beta-hydroxy-1-methyl-5 alpha-androst-1-en-3-one) greater than testosterone (T) greater than 1 alpha-methyl-DHT]. In other cases, AR binding was weak (RBA values less than 0.05): stanozolol (17 alpha-methyl-5 alpha- androstano [3,2-c]pyrazol-17 beta-ol), methanedienone (17 beta-hydroxy-17 alpha-methyl-1,4-androstadien-3-one), and fluoxymesterolone (9 alpha-fluoro-11 beta-hydroxy-17 alpha-methyl-T). Other compounds had RBAs too low to be determined (e.g. oxymetholone (17 beta-hydroxy-2-hydroxymethylene-17 alpha-methyl-5 alpha-androstan-3-one) and ethylestrenol (17 alpha-ethyl-4- estren -17 beta-ol). The competition pattern was similar in muscle and prostate, except for a higher RBA of DHT in the prostate. The low RBA of DHT in muscle was probably due to the previously reported rapid reduction of its 3-keto function to metabolites, which did not bind to the AR [5 alpha-androstane-3 alpha, 17 beta-diol and its 3 beta-isomer (3 alpha- and 3 beta-adiol, respectively)]. Some anabolic-androgenic steroids (only a few synthetic) bound to SHBG (1 alpha-methyl-DHT much greater than DHT greater than T greater than 3 beta-adiol greater than 3 alpha-adiol = 17 alpha-methyl-T greater than methenolone greater than methanedienone greater than stanozolol). The ratio of the RBA in rat muscle to that in the prostate (an estimate of the myotrophic potency of the compounds) was close to unity, varying only between about 0.4 and 1.7 in most cases.(ABSTRACT TRUNCATED AT 400 WORDS)