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From cohorts to molecules: adverse impacts of endocrine disrupting mixtures. Transcriptomics Analysis

ABSTRACT: From cohorts to molecules: adverse impacts of endocrine disrupting mixtures. Transcriptomics Analysis

PROVIDER: PRJNA720104 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14153600_1.fastq.gz	Fastqsanger.gz
	SRR14153600_2.fastq.gz	Fastqsanger.gz
	SRR14153700_1.fastq.gz	Fastqsanger.gz
	SRR14153700_2.fastq.gz	Fastqsanger.gz
	SRR14153800_1.fastq.gz	Fastqsanger.gz

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From cohorts to molecules: adverse impacts of endocrine disrupting mixtures. Transcriptomics Analysis

Project description:Convergent evidence associates exposure to endocrine disrupting chemicals (EDCs) with major human diseases, even at regulation-compliant concentrations. This might be because humans are exposed to EDC mixtures, whereas chemical regulation is based on a risk assessment of individual compounds. Here, we developed a mixture-centered risk assessment strategy that integrates epidemiological and experimental evidence. We identified that exposure to an EDC mixture in early pregnancy is associated with language delay in offspring. At human-relevant concentrations, this mixture disrupted hormone-regulated and disease-relevant regulatory networks in human brain organoids and in the model organisms Xenopus leavis and Danio rerio, as well as behavioral responses. Reinterrogating epidemiological data, we found that up to 54% of the children had prenatal exposures above experimentally derived levels of concern, reaching, for the upper decile compared with the lowest decile of exposure, a 3.3 times higher risk of language delay.

2022-02-23 | GSE171566 | GEO

A mixture of endocrine disrupting chemicals associated with lower birth weight in children induces adipogenesis and DNA methylation changes in human mesenchymal stem cells

Project description:Endocrine disrupting chemicals (EDCs) are man-made compounds that alter functions of the endocrine system. Environmental mixtures of EDCs might have adverse effects on human health, even though their individual concentrations are below regulatory levels of concerns. However, studies identifying and experimentally testing adverse effects of real-life mixtures are scarce. In this study, we aimed at evaluating an epidemiologically identified EDC mixture in an experi-mental setting to delineate its cellular and epigenetic effects. The mixture was established using data from Swedish Environmental Longitudinal Mother and child Asthma and allergy (SELMA) study where it was associated with lower birth weight, an early marker for prenatal metabolic programming. This mixture was then tested for its ability to change metabolic programming of human mesenchymal stem cells. In these cells, we assessed if the mixture induced adipogenesis and genome-wide DNA methylation changes. The mixture increased lipid droplet accumulation already at concentrations corresponding to levels measured in the pregnant women of the SELMA study. Furthermore, we identified differentially methylated regions in genes important for adipogenesis and thermogenesis. This study shows that a mixture reflecting human real-life exposure can induce molecular and cellular changes during development that could underlie adverse outcomes.

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Calretinin is a novel candidate marker for adverse ovarian effects of early life exposure to mixtures of endocrine disruptors in the rat

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Integrated transcriptome analysis of rats exposed to bisphenol mixtures from fetus to developmental stage

Project description:Bisphenol A (BPA), widely used in plastics and resins, raised health concerns for its endocrine-disrupting effects. BPA analogues like bisphenol S (BPS) and bisphenol F (BPF) emerged as alternatives but were found to exhibit similar risks. Despite many countries have implemented BPA regulations, alternatives remain insufficiently regulated Although the safety of BPS and BPF has not been sufficiently verified, they have already been detected in various surrounding environments and human urine, raising serious concerns Bisphenols are expected to have various adverse effects, but research on this is lacking. This study explores the adverse effects of bisphenol mixtures on rats from fetus to young adulthood, analyzing transcriptomes by tissue and gender to identify key genes impacted by bisphenol exposure. Dams were orally administered test substances from gestational day 6 to lactation day 6. F1 pups received the same substances at half the concentration from postnatal day 7 to day 63. The tissues collected from the pups were subjected to transcriptome analysis, and core genes were identified through integrated analysis. The study identifies core genes associated with high-density lipoprotein and hormone secretion. These genes provide insights into the mechanisms through which BPA may cause hormonal imbalances. Furthermore, the study suggests that a complex exposure of BPA, BPS, and BPF can exerts different effects than BPA alone, pronounced effects on the thyroid and reproductive organs, even though individual concentrations were below the no-observed-adverse-effect-level. It highlights the potential cumulative impact of endocrine disrupting chemicals in the body.

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Project description:Endocrine disrupting chemicals (EDCs) exert significant effects on health and physiology, many of which are traceable to effects on stem cell programming underlying organismal development. Understanding risk of low-level, chronic EDC exposure will be enhanced by knowledge of effects on stem cells. We exposed rhesus monkey embryonic stem cells to low levels of five different EDCs for 28 days, and evaluated effects on gene expression by RNAseq transcriptome profiling. EDCs tested included bisphenol A (BPA), atrazine (ATR), tributyltin (TBT), perfluorooctanoic acid (PFOA), and di-(2-ethylhexyl) phthalate (DEHP). We observed little effect of BPA, and small numbers of affected genes (119 or fewer) with the other EDCs. There was substantial overlap in effects across two, three, or four treatments. Ingenuity Pathway analysis indicated suppression of cell survival genes, activation of cell death genes, suppression of genes downstream of several stress response mediators, and modulations in several genes that regulate pluripotency, differentiation, and germ layer development. Potential adverse effects of these changes on development are discussed.

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