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At least 19 recordsLinked to original sources
PubMed1976

Induction of lactogenic receptors. II. Studies on the liver of hypophysectomized male rats and on rats bearing a growth hormone secreting tumor.

The role of growth hormone (GH), as well as prolactin and ACTH, in the induction of the PRL receptor was investigated both in hypophysectomized male rat livers and in the livers of male rats bearing a GH secreting tumor. After 7 days of s.c. injections, specific binding (% SB) of PRL in controls and rats treated with oPRL, hGH, ACTH, hCG, estradiol (E2), or testosterone (T) was approximately 1%. Treatment with oPRL plus ACTH increased SB to 4%; adding E2 to this combination produced a further increase to 8%, whereas the addition of T decreased hepatic binding to 1%. Combination of hGH with ACTH was most effective, giving a SB of 33%, which is similar to that observed in the liver of rats bearing a GH secreting tumor (36%). These studies suggest that GH acts synergistically with PRL and/or ACTH to increase lactogenic binding sites in the male rat liver and that sex steroids have a modulating effect on this action.

Adrenocorticotropic Hormone↗
PubMed1977

Effects of sex hormones on oncogenesis in rat urinary bladder by N-butyl-N-(4-hydroxybutyl)-nitrosamine.

The effects of testosterone propionate, estradiol, and estriol on the oncogenesis of male rats' bladder induced by oral administration of the carcinogen N-butyl-N-(4-hydroxybutyl)-nitrosamine (BBN) were examined. There were significant differences between the testosterone propionate-administered and estradiol-administered groups and also between the testosterone propionate-administered and estriol-administered groups in the incidence of bladder tumors.

Animals↗
PubMed1976

[Teratogenic damages of the male genital organs].

1. Malformations and functional disturbances of the male genitalia may be caused by teratogens. 2. A short review of the prenatal development points out the possible sites of action. 3. In animals some distinct teratogens produce typical malformation syndromo spermatogenetic cells. Cyproteronacetat, an antiandrogen, suppresses the development of the accessoric genital organs and produces an external feminisation. 4. In man, cryptorchidism, agenesis of the spermatic tracts, anorchia and hypospady are known as non-hereditary malformations. 5. The teratogenic etiology of some disturbances of the spermatogenesis is discussed.

Abnormalities, Drug-Induced↗
PubMed1976

Enzyme induction by oral testosterone.

Six normal male volunteers ingested a dose of 400 mg free testosterone daily as tablets over 21 days. By the end of treatment intravenous antipyrine half-life had decreased significantly from 8.0 +/- 2.7 to 5.7 +/- 2.6 hr. The subjects eliminated testosterone from serum more rapidly on the twenty-first day of testosterone ingestion than on the first day. Serum albumin, bilirubin, prothrombin, alanine-amino-transferase, and alkaline phosphatases were unchanged during the experiment. It is concluded that oral testosterone treatment induces the hepatic drug-metabolizing system including that of testosterone.

Administration, Oral↗
PubMed1977

Sexual behaviour of neonatally castrated rats injected during infancy with oestrogen and dihydrotestosterone.

Male rats were castrated on the day of birth (day 1) and injected with either testosterone, dihydrotestosterone, a synthetic oestrogen (RU 2858 + dihydrotestosterone, or oil from days 1 to 5. The aromatizable androgen, testosterone, and RU 2858 suppressed both cyclic gonadotrophin secretion, indicated by the absence of corpora lutea from implanted ovarian grafts, and the behavioural response to oestradiol benzoate + progesterone injections in adulthood. The 5alpha-reduced androgen, dihydrotestosterone alone did not affect gonadotrophin secretion or female receptive behaviour, but like testosterone, it increased penis development in response to testosterone propionate, and this was positively correlated with copulatory efficiency, i.e. the ratio of intromission to mount frequencies. Nevertheless, ejaculation only occurred among animals that had received testosterone or RU 2858 + dihydrotestosterone. The results support the concept that during the preinatal period, neural conversion of androgens to oestrogens is important both for the suppression of female gonadotrophin secretion and behaviour patterns as well as for the organization of male behaviour patterns. The 5alpha-reduction of unsaturated C19-steriods to dihydrotestosterone in peripheral tissues is also required to complete the development of the male genital tract.

Animals↗
PubMed1977

Ovulation in prenatally androgenized ewes.

The ovarian activity of prenatally androgenized ewes was studied by measuring plasma progesterone concentrations in daily samples of peripheral blood, and by examining the ovaries at laparotomy. Ewes that were exposed to testosterone between days 30 and 80, 50 and 100 or 70 and 120 of foetal life by implanting their mothers with 1 g testosterone, failed to show regular overt oestrous cycles, although some of them ovulated, whereas ewes exposed to testosterone between days 90 and 140 of foetal life had normal oestrous cycles. The incidence of ovulatory failure appeared to increase with age in ewes treated between days 50 and 100 or days 70 and 120 of foetal life.

Animals↗
PubMed1977

Progestagen effects on elicitation of aggressive behaviour in male mice.

Effects of progesterone on production of androgen-dependent aggression-eliciting pheromones were investigated. Two groups of anosmic (non-fighting) castrated mice treated with testosterone or with testosterone and progesterone, respectively, were attacked to the same degree by intact, isolated (fighting) mice while control mice (castrated only) were attacked less. The findings support the ideas that progesterone may inhibit androgen-induced aggression via a neural and not via a somatic mechanism.

Aggression↗
PubMed1976

Enzymatic responses of transplanted tumour cells towards estrogen, progesterone and testosterone.

The influence of estrogen, progesterone and testosterone on the activities of alkaline and acid phosphatases, adenosine triphosphatase and succinate dehydrogenase were determined by cytochemical methods in sarcoma 180 and Ehrlich's carcinoma cells transplanted in male and female Swiss mice. The results revealed differential effects of the sex hormones on different enzymes which seemed to depend on the type of tumour cell studied and the sex of the host mice.

Acid Phosphatase↗
PubMed1976

Inhibition of antibody-complement-mediated killing of tumor cells by hormones.

Line 1, a chemically induced guinea pig hepatoma, is susceptible to killing by anti-Forssman immunoglobulin M antibody and guinea pig complement. When these tumor cells are pretreated at 37 degrees with 10(-4) to 10(-11) M concentrations of the polypeptide hormone insulin, with the catecholamine L-epinephrine-HCl, or with the glucocorticoid steroids hydrocortisone sodium succinate or prednisolone sodium succinate, the cells show a marked reduction in their suseptibility to killing by antibody and guinea pig complement; pretreatment at 0 degrees is ineffective. Similar results were obtained with another antigenically distinct guinea pig hepatoma (line 10) when tested with anti-Forssman immuno-globulin M or specific antitumor antibodies and human complement. The ability of the hormones to render the cells resistant is dependent on time, temperature, and hormone concentration. The effect of hormone treatment is maximal between 30 and 60 min and is reversible within 4 hr even in the continued presence of hormone. Treatment of line 1 cells with up to 10,000-fold greater concentrations of the less biologically active or inactive analogs, DL-epinephrine, beta-estradiol, testosterone, or proinsulin has no effect on the susceptibility of the cells to killing by antibody and guinea pig complement. The effect of hormone treatment is not due to a direct inactivation of bound or fluid-phase complement components by the hormones or to a decrease in the ability of the cells to bind complement-fixing antibody.

Antibodies, Neoplasm↗
PubMedDate not supplied

[Effect of clomiphene on the restoration of ovulation in androgen-sterile rats].

In the androgen-sterile rats given 10-250 mug of testosterone-propionate there was observed at the early postnatal period a reduction in the LH-RP level in the hypothalamus, of the LH in the hypophysis and the blood, of the weight of the ovaries and of the corporal luteum count in them, as well as an increase in the dopamine level in the anterior portion of the hypothalamus. Klomiphen administration for 5 days in a dose of 20 mug led to the normalization of these indices and to the appearance of ovulation, but failed to restore the capacity to pregnancy. Prolonged klomiphen administration (20 mug every 3 days for a period of 1 month) also failed to restore this capacity.

Animals↗