Gestational exposure to the AhR agonist 2,3,7,8‐tetrachlorodibenzo‐<i>p</i>‐dioxin induces BRCA‐1 promoter hypermethylation and reduces BRCA‐1 expression in mammary tissue of rat offspring: Preventive effects of resveratrol

Papoutsis, Andreas; Selmin, Ornella I.; Borg, Jamie; Romagnolo, Donato F.

doi:10.1002/mc.22095

Cited by 79 publications

(70 citation statements)

References 58 publications

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“…1) [62]. This same window of epigenetic remodeling was targeted by in utero exposure to TCDD [63], which resulted in reduced BRCA-1 expression in mammary tissue of rat offspring, induced occupancy of the BRCA-1 promoter by DNA methyltransferase-1 (DNMT-1) and increased CpG methylation of the BRCA-1 promoter [63]. Some studies report cell-specific epigenetic effects of dioxins.…”

Section: Epigenetic Response To Dioxinsmentioning

confidence: 99%

Spermatogenesis disruption by dioxins: Epigenetic reprograming and windows of susceptibility

Pilsner

Parker

Sergeyev

et al. 2017

Reproductive Toxicology

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Dioxins are a group of highly persistent chemicals that are generated as by-products of industrial and natural processes. Reduction in sperm counts is among the most sensitive endpoints of dioxin toxicity. The exact mechanism by which dioxins reduce sperm counts is not known. Recent data implicate the role of epididymal factors rather than disruption of spermatogenesis. Studies reviewed here demonstrate that dioxins induce the transfer of environmental conditions to the next generation via male germline following exposures during the window of epigenetic reprogramming of primordial germ cells. Increased incidence of birth defects in offspring of male veterans exposed to dioxin containing, Agent Orange, suggest that dioxins may induce epigenomic changes in male germ cells of adults during spermatogenesis. This is supported by recent animal data that show that environmental conditions can cause epigenetic dysregulation in sperm in the context of specific windows of epigenetic reprogramming during spermatogenesis.

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Section: Epigenetic Response To Dioxinsmentioning

confidence: 99%

Spermatogenesis disruption by dioxins: Epigenetic reprograming and windows of susceptibility

Pilsner

Parker

Sergeyev

et al. 2017

Reproductive Toxicology

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show abstract

“…[52]. Additionally, prenatal exposure to the AhR ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in mice led to AhR-mediated recruitment of DNMT1 to the Brca-1 promoter and subsequent methylation and suppression of this gene [53]. The mechanisms underlying effects of EDCs on ncRNA expression have not been addressed in detail either.…”

Section: Level Of Epigenetic Regulationmentioning

confidence: 99%

Understanding Epigenetic Effects of Endocrine Disrupting Chemicals: From Mechanisms to Novel Test Methods

Alavian-Ghavanini

Rüegg

2017

Basic Clin Pharma Tox

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Endocrine-disrupting chemicals (EDCs) are man-made chemicals that interfere with hormonal signalling pathways. They are used in, for example, production of common household materials, in resin-based medical supplies and in pesticides. Thus, they are environmentally ubiquitous and human beings and wildlife are exposed to them on a daily basis. Early-life exposure to EDCs has been associated with later-life adversities such as obesity, diabetes and cancer. Mechanisms underlying such associations are unknown but are likely to be mediated by epigenetic changes induced by EDCs. Epigenetics is the study of changes in gene function that are heritable but do not entail a change in DNA sequence. EDCs have been shown to affect epigenetic marks such as DNA methylation and histone modifications. The scope of this article was to review today's knowledge about mechanisms involved in EDC-induced epigenetic changes and to discuss how this knowledge could be used for designing novel methods addressing epigenetic effects of EDCs.Since the industrial revolution, there has been a constant release of chemicals into the environment, which is linked to the increase of various health problems. A group of such environmental chemicals are endocrine-disrupting chemicals (EDCs) that interfere with the hormonal system. EDCs include a wide range of chemicals such as drugs, pesticides, plastic softeners, flame retardants. Thus, human beings and wildlife are exposed to these compounds on a daily basis, and EDCs are detectable in various body fluids [1,2].Increasing evidence suggests that EDC exposure during early life, in particular during foetal development, contributes to a variety of later-life adversaries, from cancer to cognitive impairments [3][4][5]. For instance, the synthetic oestrogen diethylstilbestrol (DES), which was given to women in the 1940s-1970s during early pregnancy to prevent miscarriages, increased the risk of a rare vaginal clear cell adenocarcinoma and infertility in the daughters (DES daughters) [6,7]. And even in the second-generation, adverse effects of DES have been reported. For example, the sons of DES daughters have increased risk of hypospadias, an abnormality of the male reproductive system [8]. It is not fully clear how chemical exposure during early development leads to persistent changes that manifest as diseases much later in life, or even in the next generation. However, increasing evidence points towards a central role for epigenetic mechanisms in these long-lasting effects of EDCs and other chemicals. Epigenetic mechanisms are responsible for permanent transcriptional regulation, and epigenetic changes can be defined as 'any long-term change in gene function that persists even when the initial trigger is long gone and that does not involve a change in gene sequence or structure' [9]. In recent years, a wealth of experimental studies and some evidence from epidemiology have demonstrated that EDCs indeed induce epigenetic changes [10].There is increasing concern in society that developmental expo...

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“…Interestingly, it was demonstrated that hexachlorobenzene modulates the crosstalk between the AhR and transforming growth factor-β1 signaling, enhancing human breast cancer cell migration and invasion [41]. Findings point to maternal exposure to AhR agonists as a risk factor for breast cancer in offspring through epigenetic inhibition of BRCA-1 expression [42]. It is hypothesized that agonists of the AhR, bisphenol A (BPA), and arsenic compounds, induce in tumor suppressor genes epigenetic signatures that mirror those often seen in sporadic breast tumors [43].…”

Section: What Are 'Estrogens'?mentioning

confidence: 99%

Adverse Effects on Female Human Reproductive Health from Exposure to Endocrine Disruptors: Focus on Endometrial Lesions

Karoutsou¹,

Karoutsos²,

Karoutsos³

2016

J Clin Epigenet

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It is currently apparent that the intentional release of compounds through agricultural, industrial, and municipal activities has influenced the health of wildlife and human populations. Scientists are invited to study disturbances in the normal function of the reproductive system of genetically modified populations. When referring to a population, they rather use the term control or reference; the reason is an enormous rate of information concerning the endocrine-altering potential of plasticizers and dyes, as well as the possible influences of pesticides and industrial compounds on various endocrine endpoints, particularly regarding the concentration of estrogens. Here in, we provide an overview on the impact of chemical substances on female human reproductive health.

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Gestational exposure to the AhR agonist 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin induces BRCA‐1 promoter hypermethylation and reduces BRCA‐1 expression in mammary tissue of rat offspring: Preventive effects of resveratrol

Cited by 79 publications

References 58 publications

Spermatogenesis disruption by dioxins: Epigenetic reprograming and windows of susceptibility

Spermatogenesis disruption by dioxins: Epigenetic reprograming and windows of susceptibility

Understanding Epigenetic Effects of Endocrine Disrupting Chemicals: From Mechanisms to Novel Test Methods

Adverse Effects on Female Human Reproductive Health from Exposure to Endocrine Disruptors: Focus on Endometrial Lesions

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