THE EFFECTS OF ANDROGENIZATION IN MALE RATS CASTRATED AT BIRTH

1966 ◽  
Vol 34 (1) ◽  
pp. 117-123 ◽  
Author(s):  
R. L. MORRISON ◽  
D. C. JOHNSON
Keyword(s):  
Testosterone Propionate ◽  
Subsequent Treatment ◽  
Male Rats ◽  
Androgen Treatment ◽  
Target Organs ◽  
Accessory Sex Organs ◽  
Increased Sensitivity ◽  
Excessive Secretion

SUMMARY Male rats were castrated on the day of birth and 5 days later half were given 2·5 mg. testosterone propionate (TP) subcutaneously (androgenization). When 30 days old, single animals were treated with graded doses of TP for 10 days. At the same time 57 males were united in parabiosis with normal intact males, and treated for 10 days with androgen. Androgenization resulted in increased sensitivity of the accessory sex organs to subsequent treatment with TP. Also, the excessive secretion of gonadotrophin by the castrated animals, as measured by androgen production in intact parabiotic partners, was more effectively inhibited by TP in androgenized than in non-androgenized males. The results are consistent with the interpretation that early androgen treatment sensitizes both the male target organs and the hypothalamo-hypophysial system to androgen.

METABOLISM AND MODE OF ACTION OF ANDROGENS IN TARGET TISSUES OF MALE RATS

1972 ◽  
Vol 69 (1) ◽  
pp. 153-164 ◽  
Author(s):  
L. Buric ◽  
H. Becker ◽  
C. Petersen ◽  
K. D. Voigt
Keyword(s):  
Skeletal Muscle ◽  
Adult Male ◽  
Mode Of Action ◽  
Total Radioactivity ◽  
Seminal Vesicles ◽  
Male Rats ◽  
Peripheral Muscle ◽  
Target Organs ◽  
Accessory Sex Organs ◽  
Testosterone Administration

ABSTRACT Either 0.7 μg [1,2-3H] testosterone* (51 Ci/mm) or 0.8 μg [1,2-3H] 5α-dihydrotestosterone (44 Ci/mm) was administered intravenously to normal adult male rats 3, 7, and 12 days after castration. 30 min after the injection, the animals were sacrificed. Total radioactivity counting was performed on aliquots of extracts of blood, peripheral muscle, prostates and seminal vesicles. In a first TCL the extracts were separated into five fractions. Further purification by acetylation and repeated chromatographic procedures revealed, that fraction C consisted of about 90 % of testosterone, fraction D of varying amounts of 5α- and 5β-DHT, fraction E of androstanedione and androstenedione, and fraction B mainly of androstanediols. The following results should be mentioned: 1. The radioactivity uptake by the accessory sex organs was significantly higher than that of skeletal muscle. The highest values were found on day 3 after castration. 5α-DHT under all conditions produced higher concentrations in the target tissues than testosterone, whereas in skeletal muscle the opposite was found. 2. After testosterone administration testosterone was very efficiently converted to 5α-DHT in target organs. Nevertheless substantial amounts of testosterone and of androstanedione and androstanediols are present. In blood, however, only small amounts of labelled 5α-DHT were found. After 5α-DHT administration, in target organs, 5α-DHT was converted to androstanedione and androstanediols up to about 20%. In blood the bulk of radioactivity was related to the androstanediol fraction. No conclusion therefore can be drawn from the data obtained in blood on the metabolic events occurring in the target organs. 3. The sequence of metabolic events in the target tissues supports the concept of a preferred 17-hydroxy pathway and a lack of 5β-reductase.

scholarly journals Androgen responsiveness of the liver of the developing rat

1974 ◽  
Vol 144 (2) ◽  
pp. 225-229 ◽  
Author(s):  
J-Å Gustafsson
Keyword(s):  
Testosterone Propionate ◽  
Neonatal Period ◽  
Female Rats ◽  
Male Rats ◽  
Second Phase ◽  
Final Phase ◽  
Male And Female ◽  
Androgen Treatment ◽  
Male And Female Rats ◽  
Developing Rat

The activities of the hepatic microsomal 2α-, 2β-, 7α- and 18-hydroxylase systems active on 5α-[4-14C]androstane-3α,17β-diol were studied in male and female rats which had been castrated at birth and at the age of 7, 13, 21, 27, 34, 43 and 55 days, treated for 5 days with 2mg of testosterone propionate/kg body weight and killed 6 days after castration. The 7α-hydroxylase system was affected very little by androgen treatment at all stages during development. On the other hand it was found that the rat liver passed through three phases during development with respect to androgen responsiveness as judged by changes in the activities of the 2α, 2β- and 18-hydroxylase systems: a first phase (from the neonatal period up to about 19 days of age) with a relative androgen unresponsiveness in both male and female rats, a second phase (from about 27 to about 33 days of age) when male and female rats responded equally well to androgens and a final phase (from about 40 days of age) with a successively decreasing androgen responsiveness in female rats but with a retained responsiveness in male rats. The hypothesis is presented that neonatal imprinting of the liver by testicular androgen(s) determines the development and degree of androgen responsiveness of liver tissue in the rat.

EFFECT OF TESTOSTERONE AND GONADOTROPHIN INJECTIONS ON THE SEX ORGAN DEVELOPMENT OF ZINC-DEFICIENT MALE RATS

1960 ◽  
Vol 38 (1) ◽  
pp. 1457-1466 ◽  
Author(s):  
M. J. Millar ◽  
P. V. Elcoate ◽  
M. J. Fischer ◽  
C. A. Mawson
Keyword(s):  
Growth And Development ◽  
Testosterone Propionate ◽  
The Other ◽  
Testicular Atrophy ◽  
Male Rats ◽  
Tubular Atrophy ◽  
Rate Of Growth ◽  
Accessory Sex Organs ◽  
Zinc Concentrations ◽  
High Concentrations

Zinc-deficient rats, receiving a diet low in zinc (0.5 μg zinc/g), were injected subcutaneously with testosterone propionate or gonadotrophins for periods of 13 to 28 days.The hormone injections in every case caused marked growth of accessory sex organs of zinc-deficient rats. The zinc concentrations of the large hormone-stimulated dorsolateral prostate glands were very low and similar to those of glands in untreated zinc-deficient rats. Testosterone propionate did not alter the testicular atrophy which had occurred before treatment. Gonadotrophin increased the rate of growth and possibly the rate of maturation of testes that were immature prior to treatment. When the testes had matured and were producing sperm before treatment, the tubular atrophy that is typical of zinc deficiency developed in spite of the injected gonadotrophins.Testicular atrophy in zinc-deficient rats is probably due specifically to an inadequate supply of zinc to the testis. The availability of sufficient zinc for incorporation of high concentrations into sperm seems to be essential for the maintenance of spermatogenesis and the survival of the germinal epithelium. On the other hand, the reduction in rate of growth and development of immature testes and of all accessory sex organs in zinc-deficient rats is due mainly to an inhibition of pituitary gonadotrophin output.

EFFECT OF TESTOSTERONE AND GONADOTROPHIN INJECTIONS ON THE SEX ORGAN DEVELOPMENT OF ZINC-DEFICIENT MALE RATS

1960 ◽  
Vol 38 (12) ◽  
pp. 1457-1466 ◽  
Author(s):  
M. J. Millar ◽  
P. V. Elcoate ◽  
M. J. Fischer ◽  
C. A. Mawson
Keyword(s):  
Growth And Development ◽  
Testosterone Propionate ◽  
The Other ◽  
Testicular Atrophy ◽  
Male Rats ◽  
Tubular Atrophy ◽  
Rate Of Growth ◽  
Accessory Sex Organs ◽  
Zinc Concentrations ◽  
High Concentrations

Zinc-deficient rats, receiving a diet low in zinc (0.5 μg zinc/g), were injected subcutaneously with testosterone propionate or gonadotrophins for periods of 13 to 28 days.The hormone injections in every case caused marked growth of accessory sex organs of zinc-deficient rats. The zinc concentrations of the large hormone-stimulated dorsolateral prostate glands were very low and similar to those of glands in untreated zinc-deficient rats. Testosterone propionate did not alter the testicular atrophy which had occurred before treatment. Gonadotrophin increased the rate of growth and possibly the rate of maturation of testes that were immature prior to treatment. When the testes had matured and were producing sperm before treatment, the tubular atrophy that is typical of zinc deficiency developed in spite of the injected gonadotrophins.Testicular atrophy in zinc-deficient rats is probably due specifically to an inadequate supply of zinc to the testis. The availability of sufficient zinc for incorporation of high concentrations into sperm seems to be essential for the maintenance of spermatogenesis and the survival of the germinal epithelium. On the other hand, the reduction in rate of growth and development of immature testes and of all accessory sex organs in zinc-deficient rats is due mainly to an inhibition of pituitary gonadotrophin output.

PERIPHERAL AND CENTRAL ANDROGENIC STIMULATION OF SEXUAL BEHAVIOUR OF CASTRATED MALE RATS

1977 ◽  
Vol 84 (4) ◽  
pp. 813-828 ◽  
Author(s):  
Rachel Hamburger-Bar ◽  
Henk Rigter
Keyword(s):  
Sexual Behaviour ◽  
Testosterone Propionate ◽  
Male Rats ◽  
Peripheral Target ◽  
Peripheral Tissues ◽  
Target Organs ◽  
The Brain ◽  
Stimulation Of ◽  
Maintenance Study

ABSTRACT The effects of androgens on the maintenance and restoration of sexual behaviour (mounts, intromissions and ejaculations) of castrated male rats were studied. In the maintenance study the rats were treated during 5 weeks, starting one day following castration. Testosterone propionate maintained sexual behaviour at an almost normal level. The androgenoestrogen intermediate 19-hydroxytestosterone propionate was unable to prevent the decline in the number of ejaculations over the weeks although this hormone maintained the post-ejaculatory refractory period in those rats that ejaculated and also maintained normal sexual latencies. In the restoration study administration of testosterone propionate during 7 weeks to long-term castrated rats restored sexual behaviour to normal. 19-Hydroxytestosterone propionate treated rats displayed mounts but no other signs of sexual behaviour. The 5α-reduced androgen dihydrotestosterone propionate did not restore sexual behaviour. Testosterone propionate and dihydrotestosterone propionate stimulated peripheral target organs; 19-hydroxytestosterone propionate was ineffective in this respect. It has been suggested that testosterone might stimulate sexual behaviour in rats in two ways, i. e., via its aromatization to oestradiol in the brain, and by stimulating growth of peripheral tissues via its 5α-reduction to dihydrotestosterone. In support for this view we have found that the combination of 19-hydroxytestosterone propionate and dihydrotestosterone propionate was effective in restoring the full pattern of sexual behaviour in castrated male rats.

scholarly journals Altered sexual differentiation of hepatic uridine diphosphate glucuronyltransferase by neonatal hormone treatment in rats

1979 ◽  
Vol 180 (2) ◽  
pp. 313-318 ◽  
Author(s):  
Coral A. Lamartiniere ◽  
Cindy S. Dieringer ◽  
Etsuko Kita ◽  
George W. Lucier
Keyword(s):  
Enzyme Activity ◽  
Adult Male ◽  
Sexual Differentiation ◽  
Reproductive Tract ◽  
Testosterone Propionate ◽  
Hormone Treatment ◽  
Male Rats ◽  
Ventral Prostate ◽  
Uridine Diphosphate ◽  
Neonatal Administration

The hepatic microsomal enzyme UDP-glucuronyltransferase undergoes a complex developmental pattern in which enzyme activity is first detectable on the 18th day of gestation in rats. Prepubertal activities are similar for males and females. However, postpubertal sexual differentiation of enzyme activity occurs in which male activities are twice those of females. Neonatal administration of testosterone propionate or diethylstilboestrol to intact animals resulted in lowered UDP-glucuronyltransferase activity in liver microsomal fractions of adult male rats, whereas no changes were observed in the adult females and prepubertal male and female animals. Neonatal administration of testosterone propionate and diethylstilboestrol adversely affected male reproductive-tract development as evidenced by decreased weights of testes, seminal vesicles and ventral prostate. Diethylstilboestrol also markedly decreased spermatogenesis. Hypophysectomy of adult male rats resulted in negative modulation of microsomal UDP-glucuronyltransferase and prevented the sexual differentiation of enzyme activity. In contrast hypophysectomy had no effect on female UDP-glucuronyltransferase activity. A pituitary transplant under the kidney capsule was not capable of reversing the enzyme effects of hypophysectomy, therefore suggesting that the male pituitary factor(s) responsible for positive modulation of UDP-glucuronyltransferase might be under hypothalamic control in the form of a releasing factor. Neonatal testosterone propionate and diethylstilboestrol administration apparently interfered with the normal sequence of postpubertal UDP-glucuronyltransferase sexual differentiation.

scholarly journals Different mechanisms of regulation of nuclear reduced nicotinamide–adenine dinucleotide phosphate-dependent 3-oxo steroid 5α-reductase activity in rat liver, kidney and prostate

1974 ◽  
Vol 142 (2) ◽  
pp. 273-277 ◽  
Author(s):  
Jan-Åke Gustafsson ◽  
Åke Pousette
Keyword(s):  
Testosterone Propionate ◽  
Reductase Activity ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Female Rats ◽  
Male Rats ◽  
Regulatory Mechanisms ◽  
Oestradiol Benzoate ◽  
Liver And Kidney ◽  
Reduced Nicotinamide Adenine Dinucleotide ◽  
Hydroxy Steroid

The regulatory mechanisms involved in the control of the nuclear NADPH-dependent 3-ketosteroid 5α-reductase (5α-reductase) activity were studied in liver, kidney and prostate. The substrate used was [1,2-3H]androst-4-ene-3,17-dione (androstenedione) (for liver and kidney) or [4-14C]androstenedione (for prostate). The hepatic nuclear 5α-reductase activity was greater in female than in male rats, was greater in adult than in prepubertal female rats, increased after castration of male rats, but was not affected by treatment with testosterone propionate or oestradiol benzoate. These regulatory characteristics are in part different from those previously described for the hepatic microsomal 5α-reductase. The renal nuclear metabolism of androstenedione, i.e. 5α reduction and 17β-hydroxy steroid reduction, was relatively unaffected by sex, age, castration and treatment with testosterone propionate. However, treatment of castrated male rats with oestradiol benzoate led to a significant increase in the 5α-reductase activity and a significant decrease in the 17β-hydroxy steroid reductase activity. Finally, the nuclear 5α-reductase activity in prostate was androgen-dependent, decreasing after castration and increasing after treatment with testosterone propionate. In conclusion, the nuclear 5α-reductase activities in liver, kidney and prostate seem to be under the control of distinctly different regulatory mechanisms. The hypothesis is presented that whereas the prostatic nuclear 5α-reductase participates in the formation of a physiologically active androgen, 5α-dihydrotestosterone, this may not be the true function of the nuclear 5α-reductase in liver and kidney. These enzymes might rather serve to protect the androgen target sites in the chromatin from active androgens (e.g. testosterone) by transforming them into less active androgens (e.g. 5α-androstane-3,17-dione and/or 5α-dihydrotestosterone).

THE EFFECT OF CERTAIN ANDROGENIC STEROIDS ON THE UPTAKE OF RADIOSULPHUR IN A HEALING FRACTURED BONE IN THE RAT

1957 ◽  
Vol 35 (1) ◽  
pp. 771-776 ◽  
Author(s):  
K. Kowalewski ◽  
R. T. Morrison
Keyword(s):  
Normal Control ◽  
Marked Effect ◽  
Testosterone Propionate ◽  
Chondroitin Sulphate ◽  
Significant Rise ◽  
Male Rats ◽  
Testosterone Administration ◽  
Androgenic Steroids ◽  
Intact Rats

The uptake of radiosulphur in the fractured and intact humerus of male rats was determined in normal and in castrated animals and the ratio F/I of radioactivity of fractured (F) to intact (I) bone was calculated. Castration resulted in a significant decrease of F/I ratio, as compared with normal control rats.The effect of testosterone propionate and 17-ethyl-19 nortestosterone (Nilevar) on the S35 uptake in bones was studied. Testosterone administration resulted in a slight increase of the F/I in castrated rats, but had no effect on this ratio in intact animals. Both castrated and intact rats treated with Nilevar exhibited a significant rise of S35 uptake in fractured bones and, consequently, high F/I ratios. It is suggested that Nilevar has a marked effect on the synthesis of chondroitin sulphate in the collagen tissues of healing fractures, as measured by the described S35 uptake technique.

Effects of intrahypothalamic crystalline steroids on acute ACTH secretion

1963 ◽  
Vol 205 (4) ◽  
pp. 671-673 ◽  
Author(s):  
Israel Chowers ◽  
Shaul Feldman ◽  
Julian M. Davidson
Keyword(s):  
Ascorbic Acid ◽  
Pituitary Gland ◽  
Median Eminence ◽  
Acute Stress ◽  
Testosterone Propionate ◽  
Experimental Period ◽  
Male Rats ◽  
Acth Secretion ◽  
Unilateral Adrenalectomy ◽  
Cortisol Implants

The respective roles of the hypothalamus and pituitary gland, in the inhibition of adrenocorticotropin secretion by corticoids, were studied by implanting small quantities of crystalline cortisol acetate in the median eminence region and pituitary of male rats. Adrenal weights and adrenal ascorbic acid depletion (AAAD) in response to the acute stress of unilateral adrenalectomy were measured 5, 10, 13, or 21 days postoperatively. Ten days following implantation in the hypothalamus, rats showed adrenal atrophy and inhibition of AAAD. Normal AAAD and slight adrenal hypertrophy were found 10 days after similar implantation of testosterone propionate in the median eminence. Animals with cortisol implants in the pituitary had normal adrenal weights and AAAD responses at this time. In rats with cortisol implants in the hypothalamus, an inhibition of AAAD was present after 5–6 days, had increased maximally at 13 days, and returned to normal at 21 days. Adrenal atrophy, however, was first noted at 10 days and adrenal weight continued to decline throughout the experimental period.

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