Developmental effects of perinatal exposure to PBDE and PCB on gene expression in sexually dimorphic rat brain regions and female sexual behavior

Faass, Oliver; Ceccatelli, Raffaella; Schlumpf, Margret; Lichtensteiger, W.

doi:10.1016/j.ygcen.2013.04.008

Cited by 29 publications

(20 citation statements)

References 43 publications

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“…Exposure of adult male mice to BPA suppressed sexual motivation and performance [129]. Other environmental agents that perturb sexual behavior include fluoxetine [130], diesel exhaust [131], PBDE and PCB [132], and a long list of environmental toxicants/pollutants (reviewed by [104]). The modes of action appear to be wide ranging, including acting as anti-androgens/androgens, activation of steroid hormone receptors [133], and inhibition of activation enzymes such as aromatase [134].…”

Section: Developmental Origins Of Adult Reproductive Dysfunction Amentioning

confidence: 99%

Environmental factors, epigenetics, and developmental origin of reproductive disorders

Cheong

Adgent

et al. 2017

Reproductive Toxicology

182

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Sex-specific differentiation, development, and function of the reproductive system are largely dependent on steroid hormones. For this reason, developmental exposure to estrogenic and anti-androgenic endocrine disrupting chemicals (EDCs) is associated with reproductive dysfunction in adulthood. Human data in support of “Developmental Origins of Health and Disease” (DOHaD) comes from multigenerational studies on offspring of diethylstilbestrol-exposed mothers/grandmothers. Animal data indicate that ovarian reserve, female cycling, adult uterine abnormalities, sperm quality, prostate disease, and mating behavior are susceptible to DOHaD effects induced by EDCs such as bisphenol A, genistein, diethylstilbestrol, p,p′-dichlorodiphenyl-dichloroethylene, phthalates, and polyaromatic hydrocarbons. Mechanisms underlying these EDC effects include direct mimicry of sex steroids or morphogens and interference with epigenomic sculpting during cell and tissue differentiation. Exposure to EDCs is associated with abnormal DNA methylation and other epigenetic modifications, as well as altered expression of genes important for development and function of reproductive tissues. Here we review the literature exploring the connections between developmental exposure to EDCs and adult reproductive dysfunction, and the mechanisms underlying these effects.

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Section: Developmental Origins Of Adult Reproductive Dysfunction Amentioning

confidence: 99%

Environmental factors, epigenetics, and developmental origin of reproductive disorders

Cheong

Adgent

et al. 2017

Reproductive Toxicology

182

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“…Winneke et al [49] found higher PCB levels to be associated with more feminine play behaviour in boys and reduced feminine play behaviour in girls. Faass and colleagues [50] found prenatal exposition to PCBs and PBDEs in rats to affect gene expression in sexually dimorphic brain areas and female sexual behaviour. Prenatal PCB exposure was also associated with a reduction of sexual behaviour in female adult rats [51,52].…”

Section: Introductionmentioning

confidence: 99%

Influence of Low-Level Prenatal Exposure to PCDD/Fs and PCBs on Empathizing, Systemizing and Autistic Traits: Results from the Duisburg Birth Cohort Study

et al. 2015

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BackgroundPolychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) and polychlorinated biphenyls (PCBs) are assumed to act as endocrine disruptor chemicals. Prenatal exposure to these pollutants might influence fetal steroid hormone levels, which are thought to be related to sex-typical development and autistic traits.ObjectivesWe examined associations of prenatal levels of PCDD/Fs and PCBs with autism traits and sex-typical behaviour in childhood.MethodsWe measured levels of PCDD/Fs and PCBs in maternal blood samples during pregnancy using gas chromatography/high-resolution mass spectrometry. Sex-typical behaviour was assessed at 9 years of age (n = 96) and autistic traits at 10 years of age using the Social Responsiveness Scale (SRS; n = 100). Multiple regression analyses were conducted to estimate the associations between prenatal exposure and outcome variables.ResultsBlood concentrations (WHO2005-TEq) of ƩPCDD/Fs ranged from 2.93–46.45 pg/g lipid base (median = 12.91 pg/g lipid base) and concentrations of ƩPCBs were in the range of 1.24–25.47 pg/g lipid base (median = 6.85 pg/g lipid base) which is within the range of German background exposure. We found significant negative associations between PCDD/F levels in maternal blood and SRS scores in the whole group (β = -6.66, p < .05), in girls (β = -10.98, p < .05) and, in one SRS subscale, in boys (β = -6.86, p < .05). For PCB levels, associations with one SRS subscale were significant for the whole study group as were associations with two subscales in girls. We did not find significant associations between PCDD/F or PCB levels and sex-typical behaviour for either sex.ConclusionsIn an earlier part of this study, prenatal exposure to PCDD/Fs and PCBs was found to be associated with lower testosterone levels, therefore, our findings are consistent with the idea that autism spectrum conditions are related to fetal androgen levels. Several possible mechanisms, through which PCDD/Fs and PCBs might influence autistic behaviour, are discussed.

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“…Differences are more than likely due to the mechanisms of action of the different compounds, dose and duration of exposure as well as other experimental differences. Finally, in the VMH of these same rats, PBDEs increased Esr1 expression in females and males (1 mg/kg dose only) and decreased Esr2 expression (Faass et al, 2013). Taken together, these data suggest that perinatal exposure to PCBs can alter estrogen receptor gene expression and protein levels in the hypothalamus but effects are region-specific.…”

Section: Dna Methylation Sexual Differentiation Of the Brain Andmentioning

confidence: 77%

“…In the rat mPOA, gestational and adolescent A1221 exposure decreased Esr1 expression in adult males but not females (Bell et al, 2016a). Conversely, polybrominated diphenyl ethers (PBDEs, 1 or 10 mg/kg given from E10–18) increased Esr1 in the mPOA of adult male and female rats, and A1254 (10 mg/kg, same days), a more highly chlorinated industrial mixture of PCBs than A1221, increased Esr2 expression in adulthood in both sexes (Faass et al, 2013). Differences are more than likely due to the mechanisms of action of the different compounds, dose and duration of exposure as well as other experimental differences.…”

Section: Dna Methylation Sexual Differentiation Of the Brain Andmentioning

confidence: 99%

Epigenetic impacts of endocrine disruptors in the brain

Walker

Gore

2017

Frontiers in Neuroendocrinology

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The acquisition of reproductive competence is organized and activated by steroid hormones acting upon the hypothalamus during critical windows of development. This review describes the potential role of epigenetic processes, particularly DNA methylation, in the regulation of sexual differentiation of the hypothalamus by hormones. We examine disruption of these processes by endocrine-disrupting chemicals (EDCs) in an age-, sex-, and region-specific manner, focusing on how perinatal EDCs act through epigenetic mechanisms to reprogram DNA methylation and sex steroid hormone receptor expression throughout life. These receptors are necessary for brain sexual differentiation and their altered expression may underlie disrupted reproductive physiology and behavior. Finally, we review the literature on histone modifications and non-coding RNA involvement in brain sexual differentiation and their perturbation by EDCs. By putting these data into a sex and developmental context we conclude that perinatal EDC exposure alters the developmental trajectory of reproductive neuroendocrine systems in a sex-specific manner.

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Developmental effects of perinatal exposure to PBDE and PCB on gene expression in sexually dimorphic rat brain regions and female sexual behavior

Cited by 29 publications

References 43 publications

Environmental factors, epigenetics, and developmental origin of reproductive disorders

Environmental factors, epigenetics, and developmental origin of reproductive disorders

Influence of Low-Level Prenatal Exposure to PCDD/Fs and PCBs on Empathizing, Systemizing and Autistic Traits: Results from the Duisburg Birth Cohort Study

Epigenetic impacts of endocrine disruptors in the brain

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