Endocrine disruptors: from Wingspread to environmental developmental biology

Markey, Caroline M.; Rubin, Beverly S.; Soto, Ana M.; Sonnenschein, Carlos

doi:10.1016/s0960-0760(02)00272-8

Cited by 181 publications

(136 citation statements)

References 61 publications

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“…Epidemiological studies suggest a positive correlation between blood levels of chemicals with estrogenic activity, such as organochlorine pollutants, and breast cancer incidence among women, implying that the growing risk of contracting mammary cancer may be linked to the wide distribution of synthetic xenoestrogens (12,13,(44)(45)(46)(47). On the other hand, beneficial health effects have been attributed to the dietary intake of natural phytoestrogens in food of plant origin (17,18).…”

Section: Discussionmentioning

confidence: 99%

“…There is also widespread concern that chemicals with estrogenic activity, for example bisphenol-A or organochlorine pollutants, may be associated with adverse health effects including cancer or other disorders of the female or male reproductive tract (9,(12)(13)(14)(15)(16). On the other hand, phytoestrogens have been proposed to confer health benefits because the high dietary intake of plant-derived estrogens, such as genistein, appears to correlate with a lower incidence of breast and prostate cancer (17,18).…”

Section: Introductionmentioning

confidence: 99%

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Convergent transcriptional profiles induced by endogenous estrogen and distinct xenoestrogens in breast cancer cells

2005

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Convergent transcriptional profiles induced by endogenous estrogen and distinct xenoestrogens in breast cancer cells

2005

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“…This new emphasis on the fetal origins of adult diseases has prompted scientists to hypothesize that fetal exposure to environmental estrogens may be the underlying cause of the increased incidence of uterine leiomyoma, testicular cancer and breast cancer observed in European and US populations over the last 50 years [3][4][5].…”

Section: Introductionmentioning

confidence: 99%

Induction of mammary gland ductal hyperplasias and carcinoma in situ following fetal bisphenol A exposure

Murray

Maffini

Ucci

et al. 2007

Reproductive Toxicology

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283

224

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Exposure of the fetus to excess estrogen is believed to increase the risk of developing breast cancer during adult life. Fetal exposure to low doses of the xenoestrogen bisphenol A resulted in long-lasting effects in the mouse mammary gland that were manifested during adult life. It enhanced sensitivity to estradiol, decreased apoptosis, increased the number of progesterone receptor-positive epithelial cells at puberty and increased lateral branching at 4 months of age. We now report that fetal exposure to 2.5, 25, 250 and 1000μg bisphenol A/kg body weight/day induces the development of ductal hyperplasias and carcinoma in situ at postnatal day 50 and 95 in rats. These highly proliferative lesions have an increased number of estrogen receptor-α positive cells. Thus, fetal bisphenol A exposure is sufficient to induce the development of preneoplastic and neoplastic lesions in the mammary gland in the absence of any additional treatment aimed at increasing tumor development.

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“…1 These xenobiotic chemicals and environmental contaminants interfere with the production, release, transport, metabolism, binding, action or elimination of natural hormones responsible for homeostasis and essential for normal growth and development. 2,3 Some EDCs are naturally occurring, for instance the flavonoids found in fruits and vegetables, and others are end products or byproducts from medicinal or industrial chemistry. Several kinds of industrial chemicals are known as environmental contaminants and examples can be found among persistent organochlorine pollutants such as DDT (1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethylene), and polychlorinated biphenyls.…”

Section: Introductionmentioning

confidence: 99%

Interference of pollutants with PPARs: endocrine disruption meets metabolism

2008

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The concept of endocrine disruption emerged over a decade ago with the observation that several natural or industrial compounds can interfere with estrogen and androgen signaling, and thereby affect both male and female reproductive functions. Since then, many endocrine-disrupting chemicals (EDCs) have been identified and the concept has been broadened to receptors regulating other aspects of endocrine pathways. In that context, interference of EDCs with receptors regulating metabolism has been proposed as a factor that could contribute to metabolic diseases such as obesity and diabetes. We review recent studies showing that several pollutants, including phthalates and organotins, interfere with PPAR (peroxisome proliferator-activated receptors) nuclear receptors and may thereby affect metabolic homeostasis. Particular emphasis is given on the mechanisms of action of these compounds. However, unlike what has been suspected, we provide evidence from mouse models suggesting that in utero exposure to the phthalate ester di-ethyl-hexyl-phthalate most likely does not predispose to obesity. Collectively, these studies define a subclass of EDCs that perturb metabolic signaling and that we propose to define as metabolic disruptors.

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Endocrine disruptors: from Wingspread to environmental developmental biology

Cited by 181 publications

References 61 publications

Convergent transcriptional profiles induced by endogenous estrogen and distinct xenoestrogens in breast cancer cells

Convergent transcriptional profiles induced by endogenous estrogen and distinct xenoestrogens in breast cancer cells

Induction of mammary gland ductal hyperplasias and carcinoma in situ following fetal bisphenol A exposure

Interference of pollutants with PPARs: endocrine disruption meets metabolism

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