UTERO-OVARIAN INTERRELATIONSHIPS IN PREPUBERAL AND GONADOTROPHS TREATED GILTS

1970 ◽  
Vol 50 (1) ◽  
pp. 185-190 ◽  
Author(s):  
G. A. SHAW ◽  
B. E. McDONALD ◽  
R. D. BAKER

Reproductive tracts from 66 prepuberal, 45 cycling and 59 gonadotrophin-treated prepuberal gilts were examined and measured to determine the effect of puberty and gonadotrophin treatment on utero-ovarian interrelationships. Occurrence of the first ovulation resulted in significant (P < 0.05) increases in uterine weight and length but not in uterine wall thickness. This change was observed after both the first spontaneous ovulation and ovulation induced by injecting 1000 IU or 2000 IU of pregnant mare’s serum (PMS) followed 48 hours later by an injection of 500 IU of human chorionic gonadotrophin. Increasing the dose of PMS from 1000 IU to 2000 IU had no effect on uterine growth. Within untreated puberal females, ovarian weight was positively (P < 0.01) correlated with uterine horn weight, length and wall thickness, whereas within prepuberal females only uterine wall thickness was correlated (P < 0.01) with ovarian weight. Seven (41%) of the 17 gilts induced to ovulate at 55 kg and slaughtered at 90 kg were cycling when slaughtered, while none of the control females were cycling. Effects of the gonadotrophin treatment on tract development in prepuberal gilts were not apparent after the first spontaneous ovulation.

1974 ◽  
Vol 75 (1) ◽  
pp. 141-147 ◽  
Author(s):  
L. J. Hipkin

ABSTRACT Dehydroepiandrosterone (DHA) augments the activity of human chorionic gonadotrophin (HCG) in the rat by increasing endogenous pituitary gonadotrophin secretion. The following experiments were undertaken to investigate the mechanism underlying this effect. Androstenedione (40 μg), dihydrotestosterone (200 μg) and testosterone (200 μg) augmented the rat uterine weight response to 0.5 IU of HCG. At these doses, the steroids did not affect basal uterine weight although this was increased when 1 mg of a steroid was injected. Androsterone (1 mg), 17α-hydroxypregnenolone (1 mg) and progesterone (200 μg) neither augmented HCG activity nor increased basal uterine weight. Ovarian weight differences were not significant in any of the experiments. Androstenedione, DHA, dihydrotestosterone and testosterone (200 μg dose level) did not significantly affect the uterine weight of castrated animals, and responses to 0.04 μg of oestradiol were not potentiated. The results with androstenedione, dihydrotestosterone and testosterone are identical to those obtained with DHA and suggest that these steroids may also increase pituitary gonadotrophin secretion.


1955 ◽  
Vol 13 (1) ◽  
pp. 59-64 ◽  
Author(s):  
P. S. BROWN

SUMMARY Two convenient bioassays of urinary gonadotrophins, using immature mice, are described. The first is based upon the initial doubling of uterine weight. The second, using the ovarian weight response, attempts to increase specificity to follicle stimulating hormone by priming with human chorionic gonadotrophin. The usefulness of both methods is discussed, and the influence of non-specific impurities during the assay of urinary extracts is stressed.


1965 ◽  
Vol 33 (3) ◽  
pp. 447-454
Author(s):  
M. J. K. HARPER

SUMMARY Administration of chlormadinone, an orally active progestational agent without significant oestrogenic activity, to intact immature female rats did not affect either ovarian or uterine weight significantly compared with controls. A single injection of human chorionic gonadotrophin (HCG) caused a 73 % increase in uterine weight in 24 hr. over the control value. This dose significantly increased ovarian weight and although it caused some stimulation of follicular development, ovulation during this time did not occur. When animals were treated with chlormadinone for 8 days, and received HCG on the 8th day, uterine weight was 170% greater than in the controls and 56% greater than with HCG alone. The uterine weight produced was similar to that found in animals treated with mestranol, a potent oestrogen, and HCG. In ovariectomized animals HCG did not affect uterine weight, while the small increase produced by chlormadinone was unaltered when HCG also was given. Mechanisms are discussed by which this augmentation of the uterine response to HCG might be produced. It seems most likely that chlormadinone administration causes storage of endogenous gonadotrophin in the pituitary, and that the exogenous gonadotrophin acts as the 'trigger' for the release of stored hormone, probably by a direct action on the hypothalamus.


1966 ◽  
Vol 35 (2) ◽  
pp. 199-206 ◽  
Author(s):  
P. S. BROWN ◽  
M. WELLS

SUMMARY The follicle-stimulating hormone (FSH) content of urinary gonadotrophic extracts was assayed by its effect on the ovarian weight of immature mice when given in conjunction with 40 i.u. human chorionic gonadotrophin. About three-quarters of all routine assays gave values of λ between 0·15 and 0·30. Precision was slightly increased when the material was given in three rather than in five injections. Correction of ovarian weight for body weight was either invalid or of no value in reducing variance. Removal of between-litter variance increased precision considerably. Mice of three randomly bred colonies were all satisfactory, and inbred C57BL mice were also suitable for the assay. C3H mice were less sensitive. The efficiency of different methods of extracting FSH from urine was examined. The method of Johnsen (1958) using precipitation with tannic acid was considered the most satisfactory and gave extracts of high potency and low bulk. Limited experiments in which purified human pituitary FSH was assayed with and without added luteinizing hormone, gave results compatible with the assumption that the method is specific for FSH.


1963 ◽  
Vol 27 (1) ◽  
pp. 77-86 ◽  
Author(s):  
J. D. HUNTER ◽  
GEORGE M. KRISE

SUMMARY Immature female albino mice were exposed to 60Co irradiation at rates of 20 r. and 40 r./day to total doses of 250,500,750 and 1000 r. Those irradiated at 40 r./day during the 1st week of life showed only one-third of the normal increase in uterine and ovarian weight after injection of human chorionic gonadotrophin (HCG) when 25 days old. No further decline in response was seen when the total dose was increased from 250 to 1000 r. Irradiation at 20 r./day to total doses of 500 r. produced little change in normal HCG response. In contrast, sexually mature adults exposed at 40 r./day to total doses of 1000 r. showed little response to HCG. Histological examination of ovaries from immature mice exposed to doses of 250, 500 and 1000 r. at 40 r./day revealed a depopulation of primary oocytes and early maturing follicles as well as a notable decrease in ovarian size.


1969 ◽  
Vol 61 (1) ◽  
pp. 89-95
Author(s):  
Rudi Borth ◽  
Annette Menzi

ABSTRACT In a study designed as a factorial experiment, the biological activity of standard solutions of human chorionic gonadotrophin in distilled water (A), saline (B), 1 % bovine serum albumin (C), 0.5 % gelatin (D), and borate buffer of pH 9 (E) was investigated under four different conditions of freezing and thawing, using the following three methods of bioassay: ovarian ascorbic acid depletion in rats (OAAD), uterine weight in mice (UW), and ovarian hyperaemia in rats (OH). Repeated freezing and thawing and prolonged storage at -15°C did not affect the potency in any test. In the OAAD test, the potency was increased 4–5fold by D, and 2–3fold by C. In the OH test, E augmented the potency 2–3fold. These findings are of interest in the practice of bioassay, in studying mechanisms of response, and regarding administration for therapeutic purposes. Diluents which possess augmenting properties could be used to improve the sensitivity of a bioassay if standard and unknowns showed the same degree of augmentation.


1970 ◽  
Vol 64 (3) ◽  
pp. 421-430
Author(s):  
L. J. Hipkin

ABSTRACT A urinary extract (GIM), which previously had been shown to inhibit small doses of human chorionic gonadotrophin (HCG) in the mouse uterus assay, was tested in the rat. In this species, GIM caused an increase in the basal uterine weight and potentiated the response to 0.1 IU HCG. Similar results, and in addition augmentation of the activity of 0.2 IU HCG, were obtained in rats injected with carbon tetrachloride or starved. GIM inhibited the activity of 0.8 IU and 1.6 IU HCG. This was thought to result from the difference in mean final body weight between the GIM and the control groups. The results support the hypothesis that GIM causes a non-specific stress reaction. In rats the effect of this is to increase endogenous gonadotrophin secretion. This contrasts with the results previously reported for mice, which suggest that stress suppresses endogenous follicle-stimulating hormone release.


1969 ◽  
Vol 60 (1) ◽  
pp. 137-156 ◽  
Author(s):  
C. Robyn ◽  
P. Petrusz ◽  
E. Diczfalusy

ABSTRACT The follicle stimulating hormone (FSH)-like activity of human chorionic gonadotrophin (HCG) preparations was assayed by the method based on the ovarian weight augmentation in intact immature rats. The potencies ranged from 4.8 to 7.4 IU equivalents of FSH per mg. The FSH-like potency of the Second International Standard Preparation of HCG was 8.5 IU per vial. However, when in intact immature rats the ovarian weight response to HCG preparations was compared at a wide range of doses (40 to 51 200 IU) to that obtained with a human menopausal gonadotrophin (HMG) preparation (0.5 to 128 IU of FSH) in the presence of 40 IU of HCG, significant differences were found. The assays conducted in hypophysectomised immature female rats were invalid, because of lack of parallelism. Antisera were prepared by immunising rabbits with HCG and human hypophysial gonadotrophin (HHG) preparations and the antigonadotrophin profiles (HCG-, FSH- and FSH-like neutralising potencies) of these antisera were established by the use of statistically valid bioassay procedures. The anti-HCG and anti-HHG sera neutralised the FSH activity of HMG preparations as well as the FSH-like activity of HCG preparations. However, 3 to 175 times more antiserum was required to neutralise the equivalent of 1.0 IU of FSH-like activity present in HCG than expected on the basis of the anti-FSH potency of the antisera. On the other hand, there was a high degree of correlation between the neutralising potencies of the antisera when tested against the FSH-like activity and the HCG activity of various HCG preparations. When the FSH-like activity of an HCG preparation was quantitatively neutralised with an anti-HCG serum, some 30 per cent of the HCG activity remained unneutralised, as evidenced by repeated bioassays. Although at least 2000 IU of this »FSH-free« HCG was administered to groups of intact as well as hypophysectomised immature female rats, this high dose of HCG did not induce an increase in ovarian weight beyond that elicited by 40 IU of untreated HCG. Histological examination of the ovaries indicated lack of follicle stimulation in the hypophysectomised, but not in the intact immature animals. There was an excessive stimulation of the interstitial cells in both types of animals. The data indicate that the FSH-like activity of HCG preparations is neither due to a contamination by FSH of pituitary origin, nor is it an evenly distributed intrinsic property of the HCG molecules. It is also concluded that the gonadotrophic activity of biologically pure HCG in immature hypophysectomised female rats consists of a specific stimulation of the interstitial cell apparatus. Such HCG preparations do not induce any follicle stimulation, not even when administered in excessive doses.


1957 ◽  
Vol 16 (1) ◽  
pp. 107-113 ◽  
Author(s):  
W. R. BUTT ◽  
A. C. CROOKE ◽  
JOYCE D. INGRAM ◽  
BRENDA P. ROUND

SUMMARY 1. Follicle stimulating hormone (FSH) has been obtained from the urine of pregnant women. 2. It was prepared by adsorption on kaolin from urine which had been treated with benzoic acid to remove excess human chorionic gonadotrophin (HCG) and was assayed by the procedure which depends on the increase in ovarian weight of immature mice treated simultaneously with HCG. 3. Preliminary results are given for the assay of FSH in normal pregnancy.


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