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D. V. SINGH and H. A. BERN


Intact female BALB/cCrgl mice, 3–4 weeks old, were pretreated with oestrogen and progesterone for 9 days. Whole mammary glands from these mice were cultivated for 5 days in a synthetic medium supplemented with aldosterone (A), prolactin (MH) and insulin (I), with and without thyroxine (T4) at concentrations ranging from 0·01 to 5 μg./ml.

A medium containing 1 μg. A +5 μg.MH +5 μg.I/ml. was generally optimal for lobulo-alveolar development. Addition of thyroxine to this combination resulted in a decrease in development which was highly significant at higher concentrations. However, when cultures were maintained in media containing suboptimal or low amounts of prolactin (1 μg. A + 3 μg. MH +5 μg. I/ml. and 1 μg. A + 1 μg. MH +5 μg. I/ml., respectively), the results indicate two possible effects of thyroxine: lower amounts of thyroxine had synergistic effects, whereas greater amounts had antagonistic effects on lobulo-alveolar development.

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VY Butnev, V Singh, VT Nguyen, and GR Bousfield

Hybrid hormone preparations were prepared by combining intact and Asn(56)-deglycosylated (N(56)dg) equine (e) LH or FSH alpha subunit preparations with truncated, des(121-149)eLH beta (eLH beta t), immunopurified, intact eLH beta or equine chorionic gonadotropin beta (eCG beta) preparations, and eFSH beta. The LH receptor-binding potencies of N(56)dg-eLH alpha:eLH beta t and N(56)dg-eFSH alpha:eLH beta t hybrids were equivalent to that of eLH; however, both N(56)dg-alpha preparations were only 3-4% as active as eLH in the rat testis Leydig cell bioassay. In the granulosa cell FSH bioassay, eLH alpha:eLH beta t stimulated progesterone synthesis and induced aromatase activity, while N(56)dg-eLH alpha:eLH beta t was completely inactive at doses up to 5 microg. N(56)dg-eLH alpha:eLH beta t inhibited progesterone production and aromatase induction elicited by 0.3 ng eFSH or 2 ng human (h) FSH. The inhibitory activities of N(56)dg-eLH alpha:eLH beta and N(56)dg-eCG alpha:eLH beta t were only 10% that of N(56)dg-eLH alpha:eLH beta t. N(56)dg-eLH alpha:eCG beta did not inhibit progesterone synthesis stimulated by eFSH at all and appeared to further stimulate aromatase induction at the highest dose tested. Preincubation of N(56)dg-eLH alpha:eLH beta and N(56)dg-eLH alpha:eLH beta t for 72 h at 37 C resulted in no loss of FSH receptor-binding activity. Preincubation resulted in 50% loss of receptor-binding activity by the eFSH preparation due to subunit dissociation, while 88% of N(56)dg-eLH alpha:eFSH beta activity was lost following 72 h, 37 C preincubation. While alpha Asn(56) oligosaccharide had no effect on eLH beta hybrid stability, it did contribute to the stability of the eFSH heterodimer.

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Endocrine Research Laboratory, Department of Obstetrics and Gynecology, Howard University Medical School, Washington D.C. 20059, U.S.A.

(Received 13 March 1978)

Cicero, Bell, Wiest, Allison, Polakoski & Robins (1975) and Mendelson, Mendelson & Patch (1975) reported that treatment of men with methadone decreases the concentration of testosterone in the blood, whereas Cushman (1973) found no significant decrease in his study. The direct effect of methadone on the capacity of the human testes to synthesize [3H]testosterone from [3H]cholesterol has therefore been investigated.

Human testicular tissue (0·5 g, obtained fresh at autopsy) was chopped with scissors and incubated with purified [1,2-3H]cholesterol (5·0 μCi, sp. act. 60 Ci/mmol; New England Nuclear Corporation, Boston, Massachusetts) in 5·0 ml Earle's medium (Difco, Detroit, Michigan) for 3 h with air as the gas phase. Co-factors were added as described by Ahluwalia, Williams & Verma (1974). Methadone hydrochloride (6-dimethylamino-4,4-diphenyl-3-heptanone hydrochloride; Eli-Lilly Co., Indianapolis, Indiana) or human chorionic gonadotrophin

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In a previous study, it was shown that thyroid hormone secretion rate (TSR) of female rats aged 55 days was reduced 22·8% by the s.c. injection of 50 μg. melatonin/day, by 14·8% when 75 μg./day was injected at 85 days, and by 9·1% when 100 μg./day was administered at 115 days (Narang, Singh & Turner, 1967). Since the rats were increasing in body weight during the period, the decrease in TSR with age may have been due to the effects of a lower dose of melatonin/g. body weight (Narang & Turner, 1966; Kumaresan & Turner, 1967). The object of the present experiment was to determine the effect of graded levels of melatonin upon the TSR of groups of rats of the same age and body weight and to determine whether melatonin has an effect on TSR of mature animals.

The TSR of 62 Sprague—Dawley—Rolfsmeyer female rats were estimated at 33

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One hundred and twenty albino female rats (Sprague-Dawley-Rolfsmeyer) were divided into five equal groups. Rates of thyroxine secretion (TSR) and food consumption were determined during the control period, and 10 and 25 days after initiation of dietary treatment. Animals in each group served as their own controls for the following modifications of their diet: (1) protein-free diet, (2) 5% protein (casein) diet, (3) 10% protein diet, (4) 15% protein diet, and (5) 20% protein diet. Purina lab chow (23·4% protein) and the 20% casein diet served as control diets. The TSR, the body weight and amount of food consumed were depressed significantly in the group fed on a protein-free diet for 10 and 25 days. The group fed 5% protein diet had a non-significant decrease in TSR as compared with the controls. Similarly, TSR was not reduced by 10, 15 or 20% protein diets. Food consumption decreased significantly in the groups fed a 5, 10 and 15% protein diet, but not in the group on 20% casein. Body weight decreased significantly in the groups on a protein-free diet and on a 5% protein diet.

It would appear from these results that protein content of the diet does not become a limiting factor for TSR until it is lower than 5%. It is suggested that the calorie intake plays a more important role in regard to TSR than a low protein content of the food.

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A Makker, F W Bansode, V M L Srivastava, and M M Singh

The role of the antioxidant defense system during endometrial receptivity, a phenomenon crucial for implantation and decidualization, and the effect of ormeloxifene, a selective estrogen receptor modulator, were investigated in the guinea pig, a laboratory mammalian species with interstitial implantation and a long functional luteal phase during each estrous cycle. A sharp rise in the activity of superoxide dismutase (SOD) in both antimesometrial (AM) and mesometrial segments and peroxidase in the AM segment of the uterus was observed on the day of maximal endometrial receptivity. Pretreatment with ormeloxifene resulted in loss of endometrial responsiveness, as evidenced by inhibition of trauma-induced decidualization and the activity of ornithine decarboxylase, a marker of tissue growth and repair. This was associated with a decrease in SOD and estradiol dehydrogenase activities, with corresponding increases in estrone dehydrogenase activity and stimulation of uterine luminal epithelial cell height and a distension of the uterine and glandular lumen. A decrease in peroxidase activity was observed only in the AM segment of the uterus on the imminent day of maximal endometrial receptivity. No effect on peripheral plasma progesterone concentration or surface ultrastructure was evident. These findings demonstrate that SOD plays an important role, with peroxidase having a supplementary role, in the first line of defense against superoxide anion radicals during the period of maximal endometrial receptivity in the guinea pig. Inhibition of endometrial receptivity and decidualization by ormeloxifene administered during the pre-receptive phase appears to be due to a depressed antioxidant defense system via dysregulation of redox-sensitive signaling, resulting in altered cellular toxicity due to increased superoxide radicals, and might contribute to the contraceptive action of ormeloxifene. This might be related to its estrogen antagonistic activity and/or decreased bioavailability of estradiol at a cellular level due to its increased metabolism to biologically less-active estrone via activation of estradiol-17 beta-hydroxysteroid dehydrogenase and suppression of estrone-17 beta-hydroxysteroid dehydrogenase.

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A. Singh, D. Hamilton-Fairley, R. Koistinen, M. Seppälä, V.H.T. James, S. Franks, and M.J. Reed


Dietary factors are known to modulate concentrations of sex hormone-binding globulin (SHBG). In the present study we have investigated the possibility that insulin like growth factor-type I (IGF-I) may be an additional regulator of SHBG using cultured human hepatoma cells which secrete SHBG. The inhibitory effect of insulin on SHBG secretion by these cells was confirmed but, in addition, IGF-I was shown to inhibit SHBG secretion by about 40% at a concentration of 100 nmol/l. A similar degree of inhibition was achieved using insulin at a concentration of 10 umol/l. Insulin, but not IGF-I, was also found to inhibit the secretion of a low molecular weight IGF-binding protein (IBP-I), which is also secreted by hepatoma cells. It is concluded that IGF-I is an additional regulator of SHBG secretion by these cells and that it may be involved in regulating SHBG secretion in vivo in response to dietary factors.