Rock Lee said:
Could you link me? I made a thread about it at CEM and everyone who replied just said which method they prefer using.
Found some:
Regulation of 3ß-Hydroxysteroid Dehydrogenase in Gonadotropin-Induced Steroidogenic Desensitization of Leydig Cells
Pei-Zhong Tang, Chon Hwa Tsai-Morris and Maria L. Dufau
Section on Molecular Endocrinology, Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20892
3ß-hydroxysteroid dehydrogenase/{Delta}5-{Delta}4 isomerases (3ß-HSD) are enzymes that catalyze the conversion of {Delta}5 to {Delta}4 steroids in the gonads and adrenal for the biosynthesis of sex steroid and corticoids. In gonadotropin-desensitized Leydig cells, from rats treated with high doses of human CG (hCG), testosterone production is markedly reduced, a finding that was attributed in part to reduction of CYP17 expression. In this study, we present evidence for an additional steroidogenic lesion induced by gonadotropin. Using differential display analysis of messenger RNA (mRNA) from Leydig cells of rats treated with a single desensitizing dose of hCG (2.5 µg), we found that transcripts for type I and type II 3ß-HSD were substantially (5- to 8-fold) down-regulated. This major reduction, confirmed by RNase protection assay, was observed at the high hCG dose (2.5 µg), whereas minor or no change was found at lower doses (0.01 and 0.1 µg). In contrast, 3ß-HSD mRNA transcripts were not changed in luteinized ovaries of pseudopregnant rats treated with 2.5 µg hCG. The down-regulation of 3ß-HSD mRNA in the Leydig cell resulted from changes at the transcriptional level. Western blot analysis showed 3ß-HSD protein was significantly reduced by hCG treatment, with changes that were coincidental with the reduction of enzyme activity and temporally consistent with the reduction of 3ß-HSD mRNA but independent of LH receptor down-regulation. The reduction of 3ß-HSD mRNA resulting from transcriptional inhibition of gene expression, and the consequent reduction of 3ß-HSD activity could contribute to the inhibition of androgen production in gonadotropin-induced steroidogenic desensitization of Leydig cells. The gender-specific regulation of 3ß-HSD by hCG reflects differential transcriptional regulation of the enzymes to accommodate physiological hormonal requirements and reproductive function.
[Kinetics of the steroidogenic response of the testis to stimulation by hCG. V. Blockade of 17-20 lyase induced by hCG is an age-dependent phenomenon inducible by pre-treatment with hCG]
[Article in French]
Forest MG, Roulier R.
The series of events, evidenced in animals after a single injection of human chorionic gonadotrophin (hCG): down-regulation of LH/hCG membrane receptors, uncoupling between receptors and the adenylate cyclase, also includes a blockade of testicular steroidogenesis beyond cyclic-AMP formation, including an inhibition of the 17 alpha-hydroxylase-17, 20-desmolase enzymatic complex. This complex phenomenon, named hCG-induced testicular desensitization also occurs in adult men. Since it is not known if and when these effects are initiated during sexual maturation, we have investigated the kinetics of responses of plasma testosterone (T), its two immediate precursors, delta 4-androstenedione (delta 4) and 17 alpha-hydroxprogesterone (OHP), and 17 beta-estradiol (E2) for a week after a single injection of hCG given at the same dosage (100 IU/kg body weight) in subjects not yet exposed to adult levels of endogenous LH, ie prepubertal boys and untreated hypogonadotrophic hypogonadic (HH) adult men. The HH subjects have been restudied after 3 months of a weekly injection of the hCG at the same dosage. In immature individuals, the effect of hCG on testicular steroidogenisis was strikingly different from that observed previously in adults: in the former, whether prepubertal boys or untreated HH adults, a single hCG injection induced a progressive and substantial rise in plasma T, maximal at 96-120 h, a modest and late rise in E2, but no significant change in delta 4 or OHP. In contrast, in adult men there is a dissociation between the responses of plasma T and delta 4 (maximal at about 72 h) to hCG and those of OHP and E2 which peak at about 24 h. After 3 months of hCG-treatment the adult pattern was induced in HH patients: early and significant rise in OHP and E2. This suggests that a pre-exposure to LH/hCG is necessary for hCG-induced testicular desensitization, at least for its enzymatic expression. A stimulatory effect of hCG on a testicular aromatase and an inhibitory effect on the 17, 20-desmolase are observed concomitantly in relation to age or to previous gonadotropin environment. It still remains uncertain to conclude that the former effect is directly responsible for the latter.
Most of the literature states that its not HCG that causes the problems but its the aromatization causes within Leydig cells by high doses of HCG for very long peroids of time. Reduce the dose to 250-500iu's and use 2x/week and the danger is relatively nonexistant.
Testicular responsiveness to chronic human chorionic gonadotropin administration in hypogonadotropic hypogonadism.
D'Agata R, Vicari E, Aliffi A, Maugeri G, Mongioi A, Gulizia S.
Steroidogenic responsiveness to long term hCG administration
(1500 U three times a week for 23 months) was characterized in 8 males with hypogonadotropic hypogonadism (HH). During hCG treatment, testosterone (T), which was in the prepuberal range under basal conditions, rose considerably to the upper end of the normal range and remained at that level during the 23 months of observation. A 2.5-fold increase was observed in serum levels of 17 beta-estradiol (E2) an increment less than seen with T. The increment in 17 alpha-hydroxyprogesterone was also lower than that in T throughout the study; thus, the 17 alpha-hydroxyprogesterone to T ratio, despite continuous hCG administration, remained low. Serum androstenedione was slightly increased during hCG therapy. No significant changes were observed in serum levels of dehydroepiandrosterone. These data indicate that continuous long term hCG administration stimulated T levels in HH, with a relatively small change in E2. The kinetics of the T and E2 responses to 2000 U hCG, evaluated after 23 months of therapy, indicated that the testicular response was markedly reduced. No increment in T levels was observed at 24 h; the maximal response occurred at 48 h. This pattern of T response supports the idea that partial testicular desensitization occurs in HH patients receiving chronic treatment with hCG.
In conclusion, use low doses 1-2/week and the problem is avoided.
