Null
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB74279 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR13244900.fastq.gz | Fastqsanger.gz | |||
| ERR13245000.fastq.gz | Fastqsanger.gz | |||
| ERR13244901.fastq.gz | Fastqsanger.gz | |||
| ERR13245001.fastq.gz | Fastqsanger.gz | |||
| ERR13244902.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Di(2-ethylhexyl) phthalate (DEHP) is a commonly used plasticizer and known endocrine disrupting chemical, which causes transgenerational reproductive toxicity in female rodents. However, the mechanisms of action underlying the transgenerational toxicity of DEHP are not understood. Therefore, this study determined the effects of prenatal and ancestral DEHP exposure on various ovarian pathways in the F1, F2, and F3 generations of mice. Pregnant CD-1 dams were orally exposed to corn oil (vehicle control) or DEHP (20 μg/kg/day-750 mg/kg/day) from gestation day 10.5 until birth. At postnatal day 21 for all generations, ovaries were removed for gene expression analysis of various ovarian pathways and for 5-methyl cytosine (5-mC) quantification. In the F1 generation, prenatal DEHP exposure disrupted the expression of cell cycle regulators, the expression of peroxisome-proliferator activating receptors, and the percentage of 5-mC compared to control. In the F2 generation, exposure to DEHP decreased the expression of steroidogenic enzymes, apoptosis factors, and ten-eleven translocation compared to controls. It also dysregulated the expression of phosphoinositide 3-kinase (PI3K) factors. In the F3 generation, ancestral DEHP exposure decreased the expression of steroidogenic enzymes, PI3K factors, cell cycle regulators, apoptosis factors, Esr2, DNA methylation mediators, and the percentage of 5-mC compared to controls. Overall, the data show that prenatal and ancestral DEHP exposure greatly suppress gene expression of pathways required for folliculogenesis and steroidogenesis in the ovary in a transgenerational manner and that gene expression may be influenced by DNA methylation. These results provide insight into some of the mechanisms of DEHP-mediated toxicity in the ovary across generations.
2020-09-22 | GSE158266 | GEO
Project description:The the ovaries of new born mouse were collected after birth and cultured in vitro with DEHP at the concentration of 0μM (vehicle control DMSO), 10μM and100μM respectively for 72 hours.Then they were performed miRNAs-seq to analyze the effects of DEHP on ovarian miRNA profile.
2019-11-23 | GSE140323 | GEO
Project description:In the present study, a pregnant mouse model exposed to di(2-ethylhexyl) phthalate (DEHP, one of the most common plasticizers) during primordial follicle formation was established. The single-cell transcriptome technology was applied to investigate the roles of melatonin in ovarian cells against DEHP exposure. .
2023-11-30 | GSE246030 | GEO
Project description:Di(2-ethylhexyl) phthalate (DEHP), a widely used plasticizer, is a ubiquitous environmental pollutant and may act as an endocrine disruptor. Early life exposures to DEHP may result in anti-androgenic effects, impairing the development of the male reproductive tract. However, data on the long-lasting consequences of such DEHP exposures on adult male reproductive function are still rare and discrepant. Previously, we identified two novel plasticizers, 1,4 butanediol dibenzoate (BDB) and dioctyl succinate (DOS), as potential substitutes for DEHP that did not reproduce classically described endocrine disrupting phenotypes in prepubertal male offspring after maternal exposure. Here, we investigated the consequences of in utero and lactational exposure to BDB and DOS on adult male rat reproductive function in a comparative study with DEHP and a commercially available alternative plasticizer, 1,2-cyclohexane dicarboxylic acid diisononyl ester (DINCH). Timed pregnant Sprague-Dawley rats were gavaged with vehicle or a test chemical (30 or 300 mg/kg/day) from gestation day 8 to postnatal day 21. While DEHP exposure (300 mg/kg/day) significantly increased epididymal weight in the adult, exposure to DINCH, BDB or DOS did not affect reproductive organ weights, steroid levels or sperm quality. Using a toxicogenomic microarray approach, we found that adult testicular gene expression was affected by exposure to the higher dose of DEHP; transcripts such as Nr5a2, Ltf or Runx2 were significantly downregulated, suggesting that DEHP was targeting estrogen signaling. Lesser effects were observed after treatment with either DINCH or BDB. DOS exposure did not produce such effects, confirming its potential as a responsible substitute for DEHP. The data deposited correspond to testicular gene expression in 90 day-old Sprague-Dawley rats after exposure to CORN OIL and 30 or 300 mg/kg/day DEHP, DINCH, BDB or DOS from gestational day 8 to post-natal day 21
2018-02-14 | GSE110553 | GEO
Project description:Di (2-ethylhexyl) phthalate (DEHP) is a common plasticizer. Studies have revealed that DEHP exposure can cause liver damage. Green tea is one of the most popular beverages in China. Green tea polyphenols (GTPs) have been proven to have therapeutic effects on organ damage induced by heavy metal exposure. However, few study report on GTP relieving DEHP-induced liver damage.
2023-10-03 | GSE232128 | GEO
Project description:Dibutyl phthalate (DBP), di-2-ethylhexyl phthalate (DEHP), and benzyl butyl phthalate (BBP) are three phthalates commonly found in consumer products, including the plastic coating of pharmaceuticals and personal care products. Folliculogenesis, a tightly regulated process occurring in the ovary, is the maturation of an immature primordial follicle to a mature antral follicle. Follicles house the oocyte and antral follicles specifically play a crucial role in ovarian steroidogenesis and ovulation. DBP, BBP, and DEHP have been associated with inhibited antral follicle growth in vitro, decreased ovulation rates in vitro, and decreased antral follicle counts in women. However, little is known about the effects of a three-phthalate mixture on antral follicles in vivo. The objective of this study was to evaluate the effects of a human relevant mixture of DBP, BBP, and DEHP on ovarian follicles through proteome profiling analysis. CD-1 female mice (60 days old) were pipet fed tocopherol stripped corn oil (vehicle control) only or a phthalate mixture (52% DBP, 36% DEHP, and 12% BBP dissolved in vehicle) which modeled human follicular fluid concentrations. The mice were treated with 32µg/kg/day (PHT Mix 32; cumulative estimate in general population) and 500µg/kg/day (PHT Mix 500; cumulative estimate in occupationally exposed individuals) for 10 consecutive days. Proteome profiling of antral follicles (>250µm) was performed via label-free tandem mass spectrometry. A total of 5,417 antral follicle proteins were identified in the three groups, of which 194 were differentially abundant between the vehicle and PHT Mix 32 group, and 136 between the vehicle and PHT Mix 500 group. Gene ontology analysis revealed that the two treatments of the phthalate mixture upregulate and downregulate distinctive processes, supporting non-monotonic effects of phthalates on the antral follicle proteome. Taken together, these results reveal that a human relevant mixture of DBP, BBP, and DEHP alters the antral follicle proteome and merits further evaluation to elucidate the molecular mechanisms by which phthalates cause negative reproductive outcomes.
2024-07-18 | PXD047061 | Pride
Project description:We investigated the impact of prenatal exposure to DEHP on spermatogenesis and DNA sperm methylation in F1 mice strains FVB/N and C57BL/6J. Prenatal exposition was performed orally on mothers with 300 mg/kg/day of DEHP from gestation day 9 to 19. 20 sperm-extracted DNA samples of males born from DEHP-treated and control mothers were analysed by MBD-seq at NXT-DX company.
2015-03-24 | GSE67159 | GEO
Project description:Introduction: In the placenta, activin A affects decidualisation and trophoblast growth and invasion. Levels increase during pregnancy to peak at parturition, while premature elevation is a hallmark of several pregnancy disorders. Here we examine the impact of elevated activin A bioactivity in the inhibin α knockout (Inha KO) mouse placenta. We also investigate whether simultaneous exposure to the endocrine disruptor, diethyl-hexyl phthalate (DEHP), which impairs normal placental function, exacerbates effects on placental morphology and gene expression in this model. Methods: Litters of Inha WT, Het and KO fetuses were collected at E15.5 from time-mated Inha heterozygous pregnant mice randomly assigned to three groups: untreated, corn oil (Vehicle) or DEHP 500 mg/kg/day, from E12.5-14.5 (n=2-17). Gross and histological placental morphology was analysed, and bulk RNA-sequencing conducted. Results: Placentae of Inha WT, Het and KO fetuses exhibited no gross differences, and no differentially expressed genes. However, sex differences included a significant increase in labyrinth area and placental size from WT males compared to WT females. DEHP exposure significantly increased fetal resorption at E15.5 but yielded little differences in placental morphology. Transcript analysis identified sex- and genotype-specific transcript alterations resulting from DEHP treatment. Eight transcripts were altered by DEHP exposure across all genotypes (Cts3, Ceacam13, Gm5155, Ssr4, Sec11c, Psg18, Psg-ps1, Taf7l). Discussion: Despite minimal morphological changes, transcriptomic differences suggest that spongiotrophoblast cells and syncytiotrophoblast giant cells are key targets of DEHP exposure, with CEA family transcripts susceptible to its effects. Additionally, DEHP exposure also modulates gene transcript responses to elevated activin A.
2025-06-12 | GSE281544 | GEO
Project description:Purpose: Then goal of this study id to investigate the effects of perinatal lead (32 ppm in maternal drinking water) and DEHP (25 mg per kg of chow) exposure on liver and blood DNA methylation in both PND21 and 5-month male and female mice. Methods: Enhanced reduced-representation bisulfite sequencing (ERRBS) was used to assess DNA methylation in PND21 and 5-month old DEHP-exposed, lead-exposed and control mice. Sex-specific differential methylaton analysis by DEHP and lead exposure was conducted using MethylSig R package. Results: We observed hundreds to thousands of stably modified, sex-specific differentially methylated regions in blood and liver of DEHP-exposed and lead-exposed animals at both PND21 and 5 months.
2020-07-01 | GSE150670 | GEO
Project description:BACKGROUND: Phthalates are manmade industrial additives used mostly as plasticizers. In addition to their deleterious effects on male genital development, population studies have recently documented correlations between phthalates exposure and subtle impacts on reproductive tract development and on the metabolic syndrome in male adults. In mature rodents liver di-(2-ethylhexyl)-phthalate (DEHP) activates the peroxisome proliferators-activated receptor (PPARalpha), a member of the nuclear receptor (NR) superfamily. OBJECTIVES: Using a systems biology approach, we aimed at defining potential mechanisms underlying the impacts of DEHP on adult mouse liver and testis. METHODS: Thus, we performed a parallel analysis of transcript and metabolic profiles in the liver from adult mice exposed to varying DEHP doses. Moreover, we obtained pangenomic mRNA profiles of laser-captured Leydig and Sertoli cells from mature animals exposed to DEHP. RESULTS: Hepatic genes modulated by DEHP are predominantly PPARalpha targets. However, the induction of some prototypic cytochrome P450 genes strongly supports the activation of additional NR pathways. Integration of hepatic transcriptomic and metabonomic profiles further revealed a correlation between the impacts of DEHP on a cluster of genes and metabolites linked to heme synthesis and on a cluster of Rev-erbalpha target genes related to metabolic and circadian clock pathways. Cell-specific effects of DEHP were investigated in the adult testis and a noticeable impact of DEHP was observed on Leydig cells transcriptome. CONCLUSIONS: We report a detailed analysis of DEHP interference with hepatic Constitutive Androstane Receptor (CAR) and Rev-erbalpha pathways and a novel transcriptional impact of DEHP on adult endocrine cells of the testis. Experiment Overall Design: two condition experiment, Sertoli cells-rich areas from DEHP-treated mice vs. Sertoli cells-rich areas from vehicle-treated mice. Biological replicates: 4 DEHP-treated samples and 4 vehicle-treated samples. Dye-swap design. N=4 DEHP-treated vs vehicle-treated x 2 microarrays (dye-swap)=8 microarrays
2009-04-10 | E-GEOD-13237 | biostudies-arrayexpress