Diethylstilbestrol and Estradiol Binding to Serum Albumin and Pregnancy Plasma of Rat and Human*

Sheehan, Daniel M.; Young, Mark

doi:10.1210/endo-104-5-1442

Cited by 106 publications

(45 citation statements)

References 27 publications

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“…The initial model used in our laboratory is the Sprague-Dawley rat given injections of 25 μg estradiol benzoate on neonatal days 1, 3 and 5 of life ( Figure 1). It is important to mention that while this is considered "high-dose", the majority of neonatally administered estradiol is bound to α-fetoprotein which circulates at high levels in neonatal rat serum (42). Consequently, neonatal estradiol is 75-fold less potent than an equivalent dose of DES (43) or, put another way, 25 μg estradiol/pup is equivalent to 0.33 μg DES/pup.…”

Section: Rat Model Of Developmental Estrogenizationmentioning

confidence: 99%

Developmental estrogen exposures predispose to prostate carcinogenesis with aging☆

Prins

Birch

Tang

et al. 2007

Reproductive Toxicology

208

162

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Prostate morphogenesis occurs in utero in humans and during the perinatal period in rodents. While largely driven by androgens, there is compelling evidence for a permanent influence of estrogens on prostatic development. If estrogenic exposures are abnormally high during the critical developmental period, permanent alterations in prostate morphology and function are observed, a process referred to as developmental estrogenization. Using the neonatal rodent as an animal model, it has been shown that early exposure to high doses of estradiol results in an increased incidence of prostatic lesions with aging which include hyperplasia, inflammatory cell infiltration and prostatic intraepithelial neoplasia or PIN, believed to be the precursor lesion for prostatic adenocarcinoma. The present review summarizes research performed in our laboratory to characterize developmental estrogenization and identify the molecular pathways involved in mediating this response. Furthermore, recent studies performed with low-dose estradiol exposures during development as well as exposures to environmentally relevant doses of the endocrine disruptor bisphenol A show increased susceptibility to PIN lesions with aging following additional adult exposure to estradiol. Gene methylation analysis revealed a potential epigenetic basis for the estrogen imprinting of the prostate gland. Taken together, our results suggest that a full range of estrogenic exposures during the postnatal critical period -from environmentally relevant bisphenol A exposure to low-dose and pharmacologic estradiol exposures -results in an increased incidence and susceptibility to neoplastic transformation of the prostate gland in the aging male which may provide a fetal basis for this adult disease.

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Section: Rat Model Of Developmental Estrogenizationmentioning

confidence: 99%

Developmental estrogen exposures predispose to prostate carcinogenesis with aging☆

Prins

Birch

Tang

et al. 2007

Reproductive Toxicology

208

162

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“…Consideration should also be given to the fact that man-made chemicals, such as DES, which bind to estrogen receptors in cells, do not bind to estrogen-binding plasma proteins (93). One function of estrogen-binding plasma proteins, such as sexsteroid binding globulin in humans, is to restrict entry of endogenous estrogen into cells (94).…”

Section: Convincing Evidence Exists That a Variety Ofmentioning

confidence: 99%

Developmental effects of endocrine-disrupting chemicals in wildlife and humans.

Colborn

Saal

Soto

1993

Environ Health Perspect

2,932

650

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Large numbers and large quantities of endocrine-disrupting chemicals have been released into the environment since World War II. Many of these chemicals can disturb development of the endocrine system and of the organs that respond to endocrine signals in organisms indirectly exposed during prenatal and/or early postnatal life; effects of exposure during development are permanent and irreversible. The risk to the developing organism can also stem from direct exposure of the offspring after birth or hatching. In addition, transgenerational exposure can result from the exposure of the mother to a chemical at any time throughout her life before producing offspring due to persistence of endocrine-disrupting chemicals in body fat, which is mobilized during egg laying or pregnancy and lactation. Mechanisms underlying the disruption of the development of vital systems, such as the endocrine, reproductive, and immune systems, are discussed with reference to wildlife, laboratory animals, and humans.

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“…This correlates with the estrogenic activities of E2 and DES estimated by the prepubertal mouse (Coldham et al 1997), although the extent of the difference was greater than the result in prepubertal mouse. The difference between the two systems may be due to the presence in vivo of binding proteins such as steroid hormone-binding globulin, which binds to DES more weakly than it binds to E2 (Sheehan & Young 1979), causing more DES to be available for ER binding. Secondly, the genes differed in their dose-dependent activation/repression patterns as we observed that the estrogens induced at least two different dose-response patterns.…”

Section: Dose-dependent Activation Of Genes By Physiological and Non-mentioning

confidence: 99%

Similarities and differences in uterine gene expression patterns caused by treatment with physiological and non-physiological estrogens

Watanabe¹,

Suzuki²,

Kobayashi³

et al. 2003

Journal of Molecular Endocrinology

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Administration of physiological and non-physiological estrogens during pregnancy or after birth is known to have adverse effects on the development of the reproductive tract and other organs. Although it is believed that both estrogens have similar effects on gene expression, this view has not been tested systematically. To compare the effects of physiological (estradiol; E2) and non-physiological (diethylstilbestrol; DES) estrogens, we used DNA microarray analysis to examine the uterine gene expression patterns induced by the two estrogens. Although E2 and DES induced many genes to respond in the same way, different groups of genes showed varying levels of maximal activities to each estrogen, resulting in different dose-response patterns. Thus, each estrogen has a distinct effect on uterine gene expression. The genes were classified into clusters according to their dose-responses to the two estrogens. Of the eight clusters, only two correlated well with the uterotropic effect of different doses of E2. One of these clusters contained genes that were upregulated by E2, which included genes encoding several stress proteins and transcription factors. The other cluster contained genes that were downregulated by E2, including genes related to metabolism, transcription and detoxification processes. The expression of these genes in estrogen receptor-deficient mice was not affected by E2 treatment, indicating that these genes are affected by the E2-bound estrogen receptor. Thus, of the many genes that are affected by estrogen, it was suggested that only a small number are directly involved in the uterotropic effects of estrogen treatment.

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Diethylstilbestrol and Estradiol Binding to Serum Albumin and Pregnancy Plasma of Rat and Human*

Cited by 106 publications

References 27 publications

Developmental estrogen exposures predispose to prostate carcinogenesis with aging☆

Developmental estrogen exposures predispose to prostate carcinogenesis with aging☆

Developmental effects of endocrine-disrupting chemicals in wildlife and humans.

Similarities and differences in uterine gene expression patterns caused by treatment with physiological and non-physiological estrogens

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