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Results for “NORETHYNODREL”

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At least 19 recordsLinked to original sources

PubMed1982

Effects of norethynodrel on neoplasms in the buccal pouch of the Syrian hamster.

This study was instituted to determine the effect of a progestin, norethynodrel, on the induction of experimental carcinogens of the hamster cheek pouch. Thirty-six Syrian hamsters were divided into two groups. One group received 2 mg./kg./day of norethynodrel in subcutaneous injections, and the other group received nothing. The right cheek pouches of both groups were painted three times a week with the chemical carcinogen 9,10-dimethyl-1,2-benzanthracene in a 0.05 percent acetone solution. After 9 weeks of painting, the first tumors developed in the hormone-treated hamsters, while none appeared in the control group until after 10 weeks. After 15 weeks, 100 percent of both groups had tumors. The average latent period was 11.8 weeks for the treated group and 12.7 weeks for the control group (p = less than 0.05 percent, Student's test). Norethynodrel significantly decreased the induction time of the neoplasms.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1977

Responsiveness to various dipsogenic stimuli in rats treated chronically with norethynodrel, ethinyl estradiol and both combined.

Administration of the estrogen, ethinyl estradiol (36 microng/kg/day), alone, and in combination with the progestogen, norethynodrel (165 microng/kg/day), significantly attenuated the dipsogenic response characteristically induced by acute s.c. administration of the beta adrenergic agonist, dl-iosproterenol (50 microng/kg). Attenuation was apparent within 1 week of steroid treatment, and remained during the 4 weeks of testing. After 16 weeks of steroid treatment, the drinking response to acute i.p. administration of renin (2 and 4 Goldblatt units/rat) was tested. The groups receiving ethinyl estradiol alone, and in combination with norethynodrel, but not norethynodrel alone, showed a reduced water intake compared with untreated controls. Drinking induced by administration of hypertonic saline (1% of body weight of 1 M NaCl solution, i.p.) was also reduced in rats treated with the estrogenic, but not the progestational, agent. However, estrogen treatment did not affect drinking after a 24-hour period of dehydration. Although the reduced dipsogenic response to isoproterenol observed in estrogen-treated rats may reflect a reduced renin secretion, drinking could not be induced in these animals by administration of renin. In addition, the reduced dipsogenic response to hypertonic NaCl loading suggests that estrogens may inhibit thirst mechanisms centrally. Dehydration, which combines hypovolemic and osmotic thirst situmul was, however, sufficient to overcome the reduced dipsogenic responsiveness of estrogen-treated rats.

Animals↗

PubMed1989

Hormone prevention of mammary carcinogenesis by norethynodrel-mestranol.

The observation that the susceptibility of the mammary gland to chemical carcinogenesis is inversely related to its level of hormonally induced differentiation led us to test whether treatment of virgin rats with an estrogenic-progestagenic hormone combination protected the gland against this carcinogenesis. Virgin Sprague-Dawley rats aged 45, 55, 65, or 75 days had implanted subcutaneously for 21 days a pellet containing norethynodrel-mestranol (NM) (98.5%-1.5%) at two doses, a physiological or low dose (LD) of 0.5 mg, equivalent to the dose used in Enovid for contraception in humans, and a pharmacological or high dose (HD) of 5.0 mg. Twenty-one days after NM pellet removal, the mammary glands of 5 animals per group were examined for the number of terminal end buds (TEBs), terminal ducts (TDs), alveolar buds (ABs) and lobules, and the DNA labeling index (DNA-LI). The remaining animals received 8 mg 7,12-dimethylbenz(a) anthracene (DMBA)/100 g body weight, and tumorigenesis was evaluated at 24 weeks. The percentage of TEBs decreased with age, and further with NM treatment at both doses. Treatment did not significantly modify the percentage of TDs, but increased that of ABs in most groups. The DNA-LI of TEBs remained constant, even during aging and after treatment, whereas both aging and treatment reduced DNA-LI in TDs and ABs. Tumor incidence declined with increasing age from 75% to 44% in the 45 and 75 day-old control groups respectively. Adenocarcinoma incidence followed the same trend. NM treatment had a dose-related protective effect against development of tumors in general and of adenocarcinomas in particular. LD treatment resulted in a marginally significant reduction in adenocarcinoma incidence, whereas HD-treated animals were 0.24 times as likely as controls to develop carcinomas. There was a statistically significant correlation between the percentage of TEBs present in the gland at the time of carcinogen administration and the incidence of adenocarcinomas. It was concluded that treatment of virgin rats with the hormone combination norethynodrel-mestranol resulted in long lasting structural changes in the mammary gland which protected this organ from a subsequent carcinogenic insult.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1977

Response of heart rate to acute administration of isoproterenol in rats treated chronically with norethynodrel, ethinyl estradiol, and both combined.

Chronic (17 to 20 weeks) administration of ethinyl estradiol alone (36 mug/kg/day), and in combination (27 or 50 mug/kg/day) with several doses of norethynodrel (135, 165 or 233 mug/kg/day), attenuated the increase in heart rate accompanying acute SC administration of the beta-adrenergic agonist, l-isoproterenol (50 or 100 mug/kg), to female rats. Dietary administration of an oral contraceptive containing mestranol and norethynodrel (7.5 mg/kg/food) was also accompanied by an attenuated response to isoproterenol. A significant inverse linear relationship was observed between the logarithm of the dose of estrogen received by each group and either heart rate or change in heart rate measured at 10, 20 and 30 min after administration of isoproterenol. Thus, the antagonistic relationship between the dose of estrogen administered chronically and responsiveness of heart rate to a test dose of isoproterenol suggests a reduced beta-adrenergic responsiveness in estrogen-treated rats.

Animals↗

PubMed1979