Bisphenol A alters early oogenesis and follicle formation in the fetal ovary of the rhesus monkey

Hunt, Patricia A.; Lawson, Crystal; Gieske, Mary C.; Murdoch, Brenda M.; Smith, Helen F.; Marre, Alyssa; Hassold, Terry; VandeVoort, Catherine A.

doi:10.1073/pnas.1207854109

Cited by 189 publications

(145 citation statements)

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“…They showed that the set of genes that is downregulated with the BPA/high-sugar diet displays a substantial increase in the number of genes highly expressed in testis ( Figure 4B and Table S2; P = 1.05e-13, Fisher's exact test). These results are in agreement with the observation that BPA impairs germline tissues (Allard and Colaiacovo 2010;Lawson et al 2011;Hunt et al 2012) and suggest that excess sugar might contribute to these toxic effects.…”

Section: Resultssupporting

confidence: 82%

“…The effects of BPA exposure on the impairment of chromosome synapsis and double-strand DNA break repair have previously been observed during Caenorhabditis elegans oogenesis (Allard and Colaiacovo 2010), and similar observations were noted in rhesus monkey females (Hunt et al 2012). Hunt et al (2012) further observed abnormal centromere associations, although the mechanisms have remained unclear.…”

Section: Widespread Consequences Of Disrupting the Ribosomal Machinerysupporting

confidence: 59%

“…BPA exposure knocks down the expression of testis-expressed genes BPA has been implicated in the disruption of a variety of reproductive traits in humans and model organisms (Allard and Colaiacovo 2010;Lawson et al 2011;Hunt et al 2012).…”

Section: Resultsmentioning

confidence: 99%

“…Hunt et al (2012) further observed abnormal centromere associations, although the mechanisms have remained unclear. One interpretation is that the spindle apparatus is directly disrupted by BPA toxicity.…”

Section: Widespread Consequences Of Disrupting the Ribosomal Machinerymentioning

confidence: 99%

“…As observed for acute exposure, the combined exposure suggests that BPA and sugar generate a distinct gene regulatory response. Interaction in the combined exposure might happen either through the independent disruption of functionally related pathways or through the enhancement of the disruption of a single pathway targeted by each individual component in the mixture.BPA exposure knocks down the expression of testis-expressed genes BPA has been implicated in the disruption of a variety of reproductive traits in humans and model organisms (Allard and Colaiacovo 2010;Lawson et al 2011;Hunt et al 2012).To address the issue in Drosophila, we investigated the consequence of the BPA/sugar interaction on gene expression levels in the testis. In agreement with expectations, chronic BPA exposure showed a statistically significant increase in the prevalence of testis-expressed genes in the set of candidates that were downregulated ( Figure 4A; P , 0.001, Fisher's exact test).…”

mentioning

confidence: 99%

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High Intake of Dietary Sugar Enhances Bisphenol A (BPA) Disruption and Reveals Ribosome-Mediated Pathways of Toxicity

Branco¹,

Lemos²

2014

Genetics

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Bisphenol A (BPA) is an organic compound to which human populations are ubiquitously exposed. Epidemiological data suggest BPA exposure might be associated with higher rates of diabetes and reproductive anomalies. Health concerns also include transgenerational consequences, but these mechanisms are crudely defined. Similarly, little is known about synergistic interactions between BPA and other substances. Here we show that acute and chronic exposure to BPA causes genome-wide modulation of several functionally coherent genetic pathways in the fruit fly Drosophila melanogaster. In particular, BPA exposure causes massive downregulation of testis-specific genes and upregulation of ribosome-associated genes widely expressed across tissues. In addition, it causes the modulation of transposable elements that are specific to the ribosomal DNA loci, suggesting that nucleolar stress might contribute to BPA toxicity. The upregulation of ribosome-associated genes and the impairment of testis-specific gene expression are significantly enhanced upon BPA exposure with a high-sugar diet. Our results suggest that BPA and dietary sugar might functionally interact, with consequences to regulatory programs in both reproductive and somatic tissues. E XPOSURE to environmental toxins is widespread. It is well documented, for instance, that human populations are commonly exposed to bisphenol A (BPA), bis(2-ethylhexyl) phthalate (DEHP), dioxins, and other organic molecules produced at industrial scales. Toxins might act by modulating epigenetic pathways to change the expression of genes and normal cellular homeostasis and could result in transgenerational consequences. The fast pace at which new compounds are invented and become ubiquitous in the environment poses a challenge to safety assessment. This challenge emerges not only from the large number of compounds to evaluate, but also from the high dimensionality of toxic responses across tissue types and developmental stages. This is further aggravated by the potential for unexpected synergism among toxins in mixtures. Sensitivity might also be strongly dependent on the specific epigenomic features and genetic makeup of an individual (Du et al. 2004).Genomic analyses have uncovered levels of human genetic variation not surmised a few decades ago (e.g., Sudmant et al. 2010). Cost-effective epigenetic and physiological models are needed for (i) addressing tissue-specific responses to toxins, (ii) gaining insights into mechanisms of epigenetic toxicity, and (iii) evaluating the manifestation of these responses across naturally occurring genotypes. In particular, cost-effective models with massive publicly available genetic information (Zwarts et al. 2011; King et al. 2012a,b;Mackay et al. 2012) might allow for genome-wide evaluation of toxic responses and assessment of coexposure outcomes in conjunction with the evaluation of unique individual responses.BPA is one of the most abundantly produced chemicals worldwide, reaching an annual volume .4 million tons (Burridge 2003). Multi...

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Section: Resultssupporting

confidence: 82%

Section: Widespread Consequences Of Disrupting the Ribosomal Machinerysupporting

confidence: 59%

Section: Resultsmentioning

confidence: 99%

Section: Widespread Consequences Of Disrupting the Ribosomal Machinerymentioning

confidence: 99%

mentioning

confidence: 99%

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High Intake of Dietary Sugar Enhances Bisphenol A (BPA) Disruption and Reveals Ribosome-Mediated Pathways of Toxicity

Branco¹,

Lemos²

2014

Genetics

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Early Developmental Programming of the Ovarian Reserve, Ovarian Function, and Fertility

Mossa

Walsh

Evans

et al. 2017

Animal Models and Human Reproduction

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The detrimental effect of microplastics on critical periods of development in the neuroendocrine system

Solleiro‐Villavicencio

León

Río-Araiza

et al. 2020

Birth Defects Research

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As a result of human socioeconomic activity, industrial wastes have increased alarmingly. Plastic pollution is globally distributed across the world due to its properties of buoyancy and durability. Two broad classes of plastic-related chemicals are of critical concern for human health-bisphenol-A or BPA, and additives used in the synthesis of plastics, which are known as phthalates. Our exposure to them is ubiquitous because they are used in the production of materials that we use daily such as polycarbonate plastics, epoxy resins, flooring, automotive parts, medical devices, dental sealants, and children's toys. Since these compounds are not covalently bound to the products, they easily leach from them, leading to high human exposure. Both, BPA and phthalates, are endocrine-disruptor compounds (EDCs) with steroidogenic activity, and can bind to different receptors, such as estrogen, androgen, PPAR-γ, and AhR. These pathways are part of the complex regulatory neuroendocrine network, since its cellular components not only express neuroendocrine receptors, but synthesize and respond to several hormones and other endocrine ligands. On the other hand, the effects of BPA and phthalates on neuroendocrine diseases have been poorly studied and the available data are inconclusive. This can be attributed to the enormous variety of animal models and the different doses used in experiments or levels found in humans. However, what is clear is that exposure to both EDCs during critical life stages induces many changes in the neuroendocrine system of exposed humans that are correlated with different reproductive and neurological diseases.

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Bisphenol A alters early oogenesis and follicle formation in the fetal ovary of the rhesus monkey

Cited by 189 publications

References 44 publications

High Intake of Dietary Sugar Enhances Bisphenol A (BPA) Disruption and Reveals Ribosome-Mediated Pathways of Toxicity

High Intake of Dietary Sugar Enhances Bisphenol A (BPA) Disruption and Reveals Ribosome-Mediated Pathways of Toxicity

Early Developmental Programming of the Ovarian Reserve, Ovarian Function, and Fertility

The detrimental effect of microplastics on critical periods of development in the neuroendocrine system

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