Effects of precocious pinealectomy and hemicastration on pituitary and plasma LH levels in immature male rats

1977 ◽  
Vol 40 (1) ◽  
pp. 33-46 ◽  
Author(s):  
A. Hus-Citharel ◽  
S. Roseau ◽  
W. Zurburg
Keyword(s):  
1933 ◽  
Vol 58 (5) ◽  
pp. 569-574 ◽  
Author(s):  
Herbert M. Evans ◽  
Edwin L. Gustus ◽  
Miriam E. Simpson

The gonadotropic hormone of the blood of the pregnant mare has been greatly concentrated by adsorption on active aluminum hydroxide followed by elution. The preparations so obtained gave demonstrable gonadotropic effects within 100 hours in 21 day old female mice following three subcutaneous injections of 0.001 mg. in 1 cc. of physiological saline. As is well known, other gonadotropic substances do not cause conspicuous development of the male gonads but injections of comparatively large doses of these preparations into immature male rats caused marked development of the testes, which in 10 days were trebled in weight. An astonishing increase in the weight of the seminal vesicles resulted, for these organs were approximately 75 times heavier than in controls.


1969 ◽  
Vol 43 (1) ◽  
pp. 105-111 ◽  
Author(s):  
D. M. DE KRETSER ◽  
K. J. CATT ◽  
H. G. BURGER ◽  
G. C. SMITH

SUMMARY Twenty-day-old male rats were injected intraperitoneally with either human luteinizing hormone (HLH) or human growth hormone (HGH) labelled with 125I. The localization of these hormones 1–2 hr. after injection was examined under the light microscope after radioautography. Major sites of localization of labelled LH were the interstitial cells of the testis and the proximal convoluted tubule of the kidney. Some hormone was also present in adipose tissue, hepatic parenchymal cells, the mesothelial lining of the peritoneum and underlying macrophages. HGH was localized principally in the proximal convoluted tubule of the kidney with some hormone present in liver, adipose tissue, and the suprarenal cortex.


1984 ◽  
Vol 103 (3) ◽  
pp. 317-325
Author(s):  
A. K. Brar ◽  
G. Fink

ABSTRACT The effects of catechol oestradiol and catechol oestrone on the release of LH and prolactin were investigated in immature male and female Wistar rats. In male rats both catechol oestradiol and catechol oestrone significantly increased the plasma concentration of LH, and catechol oestradiol but not catechol oestrone significantly increased the plasma concentration of prolactin and decreased the pituitary concentration of LH. The parent oestrogens, oestradiol-17β and oestrone, had no effect on plasma LH concentrations, but both increased significantly the plasma concentration of prolactin, and oestrone but not oestradiol-17β increased the pituitary concentration of LH. In immature female rats, catechol oestradiol inhibited the surge of LH and the increase in uterine weight induced by injecting pregnant mare serum gonadotrophin (PMSG). The injection of oestrone induced an increase in the plasma concentration of LH which was about nine times greater than that produced by oestradiol-17β. There were no significant differences in the effects of these steroids on plasma prolactin concentration. These results (i) confirm that in the immature male rat catechol oestrogens can stimulate LH release and show that catechol oestradiol can increase prolactin release, (ii) show that catechol oestradiol can inhibit the stimulatory effects of PMSG on LH release and uterine weight in the immature female rat, and (iii) demonstrate that oestrone can stimulate LH release in the immature female rat. J. Endocr. (1984) 103, 317-325


Endocrinology ◽  
1933 ◽  
Vol 17 (3) ◽  
pp. 295-298 ◽  
Author(s):  
MILTON MOLIEN ◽  
FRED E. D’AMOUR ◽  
R. G. GUSTAVSON
Keyword(s):  

2006 ◽  
Vol 28 (2) ◽  
pp. 252-258 ◽  
Author(s):  
C. Li ◽  
S. Taneda ◽  
A. K. Suzuki ◽  
C. Furuta ◽  
G. Watanabe ◽  
...  

1976 ◽  
Vol 81 (1) ◽  
pp. 73-81 ◽  
Author(s):  
Jesus A. Vilchez-Martinez ◽  
Akira Arimura ◽  
Andrew V. Schally

ABSTRACT The effect of Actinomycin D (Act D) on the release of LH and FSH induced by LH-RH was investigated in rats. Immature male rats received an iv infusion over a period of 3–4 h or a quick iv injection of synthetic LH-RH. Infusion of LH-RH significantly increased serum LH and FSH levels at 1, 2, 3 and 4 h after the initiation of infusion. Pre-treatment with 100 μg/100 g b. w. Act D failed to affect the rise of serum LH and FSH levels 1 h after the infusion but significantly suppressed the response at 2, 3 and 4 h. The increase in serum LH and FSH levels after a quick injection of LH-RH was unaffected by pre-treatment with Act D whether the antibiotic was injected 1 or 2 h before LH-RH. The results suggest that the initial phase of the pituitary response to LH-RH does not require DNA-dependent RNA synthesis, whereas that in the later period does. RNA synthesis may be necessary only to maintain the increased secretion of both LH and FSH during a continuous stimulation with LH-RH.


1966 ◽  
Vol 121 (3) ◽  
pp. 803-804 ◽  
Author(s):  
J. N. Panda ◽  
C. W. Turner

1974 ◽  
Vol 52 (9) ◽  
pp. 744-750 ◽  
Author(s):  
W. H. Moger ◽  
D. T. Armstrong

Treatment of hypophysectomized immature male rats with luteinizing hormone (LH) greatly increased the metabolism of both 4-[14C]progesterone and 4-[14C]testosterone by testicular homogenates. Prolactin, either alone or in combination with LH, did not influence the metabolism of either substrate. Progesterone was metabolized to 17α-hydroxyprogesterone, androstenedione, 5α-pregnan-3,20-dione, 3α-hydroxy-5α-pregnan-20-one, and 3β-hydroxy-5α-pregnan-20-one. Testosterone was metabolized to dihydrotestosterone and 5α-androstan-3α,17β-diol. On the basis of these observations it is suggested that LH stimulated the 5α-reductase(s) of the immature rat testis. Testis homogenates from immature rats with intact pituitaries were incubated with 4-[14C]3α-hydroxy-5α-pregnan-20-one. Rapid conversion to androsterone was observed, with the formation of a compound chromatographically identical with 3α, 17α-dihydroxy-5α-pregnan-20-one as an apparent intermediate. These findings demonstrate the ability of the rat testes to form androsterone from progesterone by a pathway that does not involve testosterone.


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