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Results for “DIETHYLSTILBESTROL”

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At least 1,225 records · Page 68Linked to original sources
PubMed2004

Developmental exposure to diethylstilbestrol (DES) alters uterine response to estrogens in prepubescent mice: low versus high dose effects.

Outbred CD-1 mice received subcutaneous injections on neonatal days 1-5 with DES (0.0001-1000 microg/kg per day), a model xenoestrogen. At 17 days of age, uterine wet weight increase in response to estrogen was altered in neonatally DES-treated mice compared to controls. The response varied depending on the neonatal DES dose; a low dose (0.01 microg/kg) caused an enhanced uterine response but higher neonatal doses dampened the response. Western blots and immunolocalization of estrogen receptor alpha (ERalpha) showed high ER levels at DES 0.01 microg/kg, but decreased levels at higher doses compared to controls. Genes responding through ER-mediated pathways (c-fos, proliferating cell nuclear antigen (PCNA), and lactoferrin (LF)) mirrored altered wet weight responses, i.e., enhancement at low doses and dampening at higher doses. A similar dose-response curve was seen in 4 months old ovariectomized DES-treated mice suggesting the altered response was long-term. These data suggest xenoestrogen exposure during critical developmental windows alters hormone programming so that the uterus responds abnormally to estrogen later in life, and that the response differs following high versus low doses of neonatal exposure.

Animals↗
PubMedDate not supplied

Prenatal diethylstilbestrol (DES) exposure is associated with uterine leiomyoma development.

Early life exposure to DES causes uterine leiomyomata in laboratory animals. We examined the relationship between prenatal DES exposure and development of uterine leiomyomata in women. Among randomly selected study participants (819 black women, 504 white women), leiomyoma status was determined by ultrasound screening (70%) or surgical record review (7%). We relied on self-report of prior diagnosis in 13%. Leiomyoma status could not be ascertained for 10% and they were excluded from analyses. Prenatal DES exposure was assessed by interview. All five of the black women who reported DES exposure had leiomyomata. Among white women, 76% who reported prenatal DES exposure had leiomyomata compared with 52% of the unexposed (adjusted odds ratio for whites: 2.4; 95% confidence interval CI: 1.1-5.4). Exposed women tended to have larger tumors. Results were robust to sensitivity analyses. Findings support experimental animal data and indicate a role for prenatal estrogen exposure in the etiology of human uterine leiomyoma.

Adult↗
PubMed2005

Diethylstilbestrol-induced prolactinoma: dose-related tumor growth and effect of catecholaminergic cells on prolactin tumor cells.

BACKGROUND: Prolactinoma is a pituitary adenoma originating from prolactin-secreting epithelial cells of the adenohypophysis. Unfortunately, there appears to be a relatively high recurrence rate despite all pharmacological, radiological, and surgical therapeutic interventions. The aim of the present study was to evaluate the extent of involvement of the dopaminergic dysregulation hypothesis of prolactinomas. We transplanted, in rats, DES-induced prolactinoma cells into the adrenal medulla or under the renal capsule, two tissues rich and poor in catecholaminergic innervation, respectively. METHODS: Prolactinoma was dose-dependently induced in ovariectomized female rats implanted with 10 and 20 mg DES, and tumor cells taken from prolactinoma induced by 20 mg DES were either transplanted under the renal capsule or into the adrenal medulla. RESULTS: Although the adrenal medulla, with its high dopamine content to inhibit prolactin secretion, was devoid of any tumoral development, a significant tumoral development was evident under the renal capsule, seemingly because of no inhibitory control over prolactin secretion coexisting with the dopamine deficiency of the tissue. Results are discussed for an alternatively possible regression and prevention of any relapse of prolactinoma, most possibly occurring because of tuberoinfundibular dopamine deficiency, by the implantation of another dopamine-rich tissue beside the tumoral mass. CONCLUSION: Regression and prevention of any relapse of a tumoral outgrowth, most possibly occurring because of tuberoinfundibular dopamine deficiency, can well be alternatively achieved by the implantation of another dopamine-rich tissue beside the tumoral mass prolactinoma.

Adrenal Medulla↗