A comparative study of the actions of tamoxifen, estrogen and progesterone in the ovariectomized rat

Kalu, Dike N.; Salerno, Elena; Liu, C.C.; Echon, R.; Ray, Michelle; Garza-Zapata, M.; Hollis, Bruce W.

doi:10.1016/0169-6009(91)90002-h

Cited by 87 publications

(43 citation statements)

References 29 publications

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“…It is known that ovariectomy in the rat causes an increase in weight gain and that this is completely prevented by estrogens and tamoxifen (5). This is confirmed in our study where body weight gain was significantly higher in ovariectomized rats as compared to sham-operated controls.…”

Section: Discussionsupporting

confidence: 81%

“…In order to provide direct evidence on the relationship between collagen glycosylation of trabecular bone and estrogens, the ovariectomized animals were treated with either 17ß-estradiol or with the partial agonist of the estrogen receptor, tamoxifen (5,6). This paper, which is a continuation of the previous one (1), reports the results obtained in this investigation.…”

Section: Introductionsupporting

confidence: 60%

See 1 more Smart Citation

17β-Estradiol and Tamoxifen Prevent the Over-Glycosylation of Rat Trabecular Bone Collagen Induced by Ovariectomy

Moro¹,

Bettica²,

Romanello³

et al. 1997

CCLM

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Summary:We have recently demonstrated that ovariectomy in the rat causes over-glycosylation of collagen which is restricted to trabecular bone. In order to obtain further evidence, we studied whether estrogen or tamoxifen treatment prevented over-glycosylation of trabecular bone collagen. Forty one-hundred-day-old female rats were subjected to ovariectomy (n = 30) or sham-operation (n = 10). Starting the day of the operation, sham-operated rats were treated with vehicle, while ovariectomized rats were divided into three groups and treated with vehicle (n = 10), estrogen (n = 10) or tamoxifen (n = 10). Five rats from each group were sacrificed at 115 and 145 days of age. Femurs and tibiae were separated into cortical and trabecular bone, demineralized, hydrolyzed and analyzed by HPLC for hydroxylysine glycosides and hydroxyproline content. Hydroxylysine glycoside content was expressed as a molar ratio with hydroxyproline. The results can be summarized as follows: 1) cortical bone collagen glycosylation did not vary among the different groups;2) over-glycosylation of trabecular bone collagen observed in the ovariectomized rats was prevented by the administration of either 17ß-estradiol or tamoxifen.These data demonstrated that estrogens affect glycosylation of trabecular bone collagen.

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Section: Discussionsupporting

confidence: 81%

Section: Introductionsupporting

confidence: 60%

17β-Estradiol and Tamoxifen Prevent the Over-Glycosylation of Rat Trabecular Bone Collagen Induced by Ovariectomy

Moro¹,

Bettica²,

Romanello³

et al. 1997

CCLM

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“…In this study, bone density and uterine weight were measured in animals receiving treatment with tamoxifen and letrozole in a preclinical model. Consistent with data from others (28,29), we show that tamoxifen treatment promotes BMD (Table 1) and uterine hypertrophy (Fig. 2).…”

Section: Discussionsupporting

confidence: 80%

Effects of the Antiestrogen Tamoxifen and the Aromatase Inhibitor Letrozole on Serum Hormones and Bone Characteristics in a Preclinical Tumor Model for Breast Cancer

Núñez¹,

Jelovac

Macedo

et al. 2004

Clinical Cancer Research

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Purpose: The purpose of this study was to evaluate and compare the effects of the antiestrogen tamoxifen and the aromatase inhibitor letrozole on tumor growth, serum hormones, uterine weight, body composition, and bone characteristics in mice.Experimental Design: Human estrogen-dependent breast cancer cells stably transfected with the aromatase gene (MCF-7CA cells) were inoculated in Matrigel subcutaneously into ovariectomized nude mice. This model represents postmenopausal breast cancer in many respects, including the fact that estrogen is no longer produced by the ovaries and is not under feedback regulation by gonadotropins. Mice that received subcutaneously implanted MCF-7CA cancer cells were then treated with tamoxifen or letrozole for 7 weeks.Results: As reported previously, tumor growth was markedly inhibited by both tamoxifen (100 g/day) and letrozole (10 g/day). Tamoxifen treatment led to increased bone mineral density (BMD) and hyperplastic uteri. Mice treated with letrozole had significantly smaller uteri than the controls and tamoxifen-treated mice. Letrozole did not affect BMD. There was no significant difference in systemic leptin and insulin-like growth factor I levels as a result of tamoxifen or letrozole treatment. Conclusions:Tamoxifen treatment inhibited breast cancer cell growth and increased BMD but caused uterine hypertrophy in this preclinical model of postmenopausal breast cancer. Letrozole inhibited tumor growth without inducing uterine hypertrophy. In addition, letrozole had no effect on BMD. These findings provide experimental evidence that letrozole is an effective and safe (in terms of risk of endometrial cancer risk and osteoporosis) alternative or complement to tamoxifen treatment for breast cancer.

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“…Estrogen prevents bone loss in this animal model by reducing bone turnover (18)(19)(20)(21)(22) while PTH, given intermittently, acts as an anabolic agent for bone formation (23)(24)(25)(26)(27)(28)(29). In this study, we present data on changes in bone mass, as well as trabecular connectivity, as a result oftreatment ofOvx animals with estrogen and/or PTH.…”

Section: Introductionmentioning

confidence: 92%

Loss of cancellous bone mass and connectivity in ovariectomized rats can be restored by combined treatment with parathyroid hormone and estradiol.

Shen¹,

Dempster²,

Birchman³

et al. 1993

J. Clin. Invest.

172

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To evaluate the potential use of a combination of antiresorption and bone formation-promoting agents as a treatment for postmenopausal osteoporosis, we examined the effects of combined and separate administration of estrogen ( 17,8-estradiol, 30 ;Lg/ kg per d, s.c.) and parathyroid hormone (rPTH 40 ;&g/ kg per d, s.c.) on the proximal tibia of ovariectomized (Ovx) rats. The treatments lasted for 4 wk and were initiated 1, 3, and 5 wk after surgery. Ovx resulted in rapid loss of cancellous bone volume (Cn-BV/TV) as well as trabecular connectivity, as determined by two dimensional strut analysis. When administered in a preventive mode, treatment beginning I wk postOvx, estrogen or PTH treatment alone preserved Cn-BV/TV and trabecular connectivity, and combined estrogen and PTH treatment caused a 40% increment in Cn-BV/TV while maintaining comparable trabecular connectivity with that seen in the Sham-operated animals. When administered in a curative mode to rats with established osteoporosis, treatments beginning 3 or 5 wk post-Ovx, estrogen or PTH treatment alone prevented further loss of connectivity and Cn-BV/TV, whereas the combined treatment resulted in as much as a 300% improvement in one of the parameters of trabecular connectivity, node to node strut length, and a 106% increase in Cn-BV/TV, with respect to the bone status at the initiation of treatment. The beneficial effects of this combined treatment derive from estrogen's ability to prevent accelerated bone resorption and, simultaneously, PTH's promotion of bone formation. These data demonstrate, in an animal model, that therapies can be devised to cure the skeletal defects associated with established osteoporosis. (J.

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A comparative study of the actions of tamoxifen, estrogen and progesterone in the ovariectomized rat

Cited by 87 publications

References 29 publications

17β-Estradiol and Tamoxifen Prevent the Over-Glycosylation of Rat Trabecular Bone Collagen Induced by Ovariectomy

17β-Estradiol and Tamoxifen Prevent the Over-Glycosylation of Rat Trabecular Bone Collagen Induced by Ovariectomy

Effects of the Antiestrogen Tamoxifen and the Aromatase Inhibitor Letrozole on Serum Hormones and Bone Characteristics in a Preclinical Tumor Model for Breast Cancer

Loss of cancellous bone mass and connectivity in ovariectomized rats can be restored by combined treatment with parathyroid hormone and estradiol.

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