Prenatal DBP Exposure Dysregulate Fetal-Placenta Staptial Treanscriptomic Profiles
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE333401 | GEO | 2026/07/11
REPOSITORIES: GEO
Similar Datasets
Project description:High dose level dibutyl phthalate (DBP) exposure of fetal rat testes in vivo inhibits testosterone production (i.e. endocrine disruption). Here, fetal testis mRNA levels were profiled following exposure to a DBP dose level that did not significantly reduce testosterone levels. The goal was to identify the constellation of gene expression changes that do not correlate with endocrine disruption.
2011-04-25 | GSE25196 | GEO
Project description:Dibutyl phthalate (DBP) and diisobutyl phthalate (DiBP) have been reported to exhibit reproductive toxicity and may pose a threat to their offspring. However, the combined effect of DBP and DiBP on offspring remains unclear, especially for aquatic organisms. The aims of this study were to assess the effects of parental combined exposure to DBP and DiBP on early development of zebrafish offspring, and to explore the potential molecular mechanisms involved. The early developmental indicators and transcriptomic profiles of F1 larvae were examined after parental exposure to DBP, DiBP and their mixtures (Mix) for 30 days. Results showed that parental exposure to DBP and DiBP, alone or in combination, resulted in increasing hatchability at 48 hpf and heart rate at 96 hpf, and affected the malformation and mortality in F1 larvae. Generalized linear model (GLM) indicated that the interactive effects between DBP and DiBP on the mortality and malformation of F1 larvae was antagonistic. The transcriptomic analysis predicted that the molecular mechanisms of parental combined exposure were different from those of either chemical alone, disruption of the molecular function involving unfolded protein binding, E-box binding and photoreceptor activity in F1 larvae could be the mechanism of action after parental combined exposure.
2020-12-29 | GSE147715 | GEO
Project description:Several studies have reported an association between phthalate exposure and an increased risk of atopic dermatitis (AD). However, the molecular mechanism underlying this phenomenon in children remains unknown. In this study, we investigated the effect of Dibutyl Phthalate (DBP), one of the phthalate, on AD development and explored the potential mechanisms using proteomics.
2026-06-20 | PXD053710 | Pride
Project description:High dose level dibutyl phthalate (DBP) exposure of fetal rat testes in vivo inhibits testosterone production (i.e. endocrine disruption). Here, fetal testis mRNA levels were profiled following exposure to a DBP dose level that did not significantly reduce testosterone levels. The goal was to identify the constellation of gene expression changes that do not correlate with endocrine disruption. Fischer 344 rats were exposed via oral gavage of the dam to vehicle (corn oil) or 50 mg/kg (body weight) DBP daily from gestational day (GD) 12 to 20. The day after mating was defined as gestational day 0. Six hours after the final exposure on GD20, fetal testes were dissected and mRNA levels quantified using Affymetrix Rat Expression 230 2.0 microarrays.
2011-04-25 | E-GEOD-25196 | biostudies-arrayexpress
Project description:Phthalates are widely used as industrial plasticisers in the manufacture of plastics, resins, rubbers, paints, emulsifiers, medical devices, personal care products, and so on. Diethylhexyl phthalate (DEHP) and dibutyl phthalate (DBP) are the most common members of the phthalate group. As typical peroxisome proliferators, plasticisers and their derivatives have been shown to induce fatty liver in rodents by interfering with peroxisome proliferator-activated receptors (PPARa) (Feige et al. 2010; Issemann and Green 1990). In this study, the effects of plasticisers on hepatic glycolipid metabolism were investigated using a human liver organoid to explore the endocrine-disrupting effects of plasticisers and their mechanisms in a state more closely resembling that of a real human organ.
2026-03-23 | GSE293605 | GEO
Project description:Aquatic organisms are generally exposed to a mixture of phthalate esters (PAEs) that have been shown to induce reproductive toxicity. However, their potential toxicity mechanisms to aquatic organisms remain unclear. Here male zebrafish were exposed to dibutyl phthalate (DBP), diisobutyl phthalate (DiBP) and their mixtures for 30 days, and their effects on plasma sex hormones, testis histology and testis transcriptomics were investigated. DBP, DiBP and their mixtures could induce the disequilibrating ratio of testosterone (T) and plasma estradiol (E2) in plasma. The percentage of spermatozoa (Sz) was significantly decreased by 30.6% under DBP-1133 exposure and 27.8% under Mix-3 exposure, and widen intercellular spaces appeared under DiBP-1038 exposure. Transcriptome sequencing revealed 2795 differentially expressed genes (DEGs) in the DBP-1133 exposure group, 1613 DEGs in the DiBP-1038 exposure group and 4570 DEGs in the Mix-3 exposure group, indicating that the toxicity of combined exposure was higher than that of single exposure. Cytokine-cytokine receptor interaction was associated with the toxicity mechanism of DBP, DiBP and Mix. While GnRH signaling pathway and MAPK signaling pathway were related to the toxicity mechanism of DBP. ECM-receptor interaction, steroid hormone biosynthesis, retinol metabolism and PPAR signaling pathway were associated with the toxicity mechanism of DiBP and Mix.
2021-09-30 | GSE136994 | GEO
Project description:Provided later Pregnant Fisher 344 rats will be purchased from Charles River Laboratories, Inc. and delivered to CIIT on gestational day (GD) 7 (GD0 = day first vaginal plug positive). At gestational day 12 (GD12), the dams will be exposed once/day until GD20 to 50 mg/kg dibutyl phthalate (DBP) in corn oil vehicle via oral gavage. Each dose group will contain 4-6 vehicle control or phthalate treated dams. Groups of animals will be sacrificed at GD20, postnatal day (PND) 35, and PND90 for endpoint analysis. At GD20, treated and control animals will be examined for various endpoints including body weight, testicular histopathology, gene expression profile via microarray analysis, and anogenital distance (AGD). AGD (at parturition; PND1) and nipple number/location (at PND14 and day of sacrifice) will be determined on animals in the postnatal groups. At PND35 or 90, one male from each in utero corn oil vehicle or DBP exposed group will receive a second gavage of either corn oil or 500 mg/kg DBP. 6 hours after the second gavage, the following endpoints will be examined: 1) testis histopathology; 2) spermatid head quantification (PND90 only); 3) testis and body weights; 5) genome-wide gene expression (via microarray); and 6) germ cell apoptosis (TUNEL assay).
2008-11-24 | E-GEOD-13550 | biostudies-arrayexpress
Project description:Phthalate esters (PAEs), a notable plasticizer, could be prolific contaminants in the aquatic environment, and have been shown to induce reproductive toxicity. However, studies concerning the toxicity towards aquatic species are based upon individual chemicals and the combined toxicity of PAEs to aquatic organisms remains unclear. The aim of this study was to explore the potential toxic mechanism of combined exposure to dibutyl phthalate (DBP) and diisobutyl phthalate (DiBP) in adult female zebrafish ovarian. Zebrafish were exposed to DBP, DiBP and their mixtures for 30 days, and their effects on ovarian histology, plasma sex hormones and ovarian transcriptomics were investigated. The plasma estradiol (E2) levels were significantly decreased 38.9% for DBP-1133 exposure group and 41.0% for DiBP-1038 exposure group. The percentages of late/mature oocyte were also significantly decreased 17.3% in DBP-1133 exposure and 16.2% in DiBP-1038 exposure, while those in combined exposure were not significantly affected. Nonetheless, transcriptome sequencing discovered 2564 differential expressed genes (DEGs) in zebrafish ovary after exposure to the mixtures. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis identified that those DEGs were involved in the neuroactive ligand-receptor interaction, GnRH, progesterone-mediated oocyte maturation, oocyte meiosis and steroid hormone biosynthesis signaling pathways. These results revealed that combined exposure showed potential reproductive toxicity at the molecular level.
2019-08-27 | GSE134345 | GEO
Project description:Environmental compounds are known to promote epigenetic transgenerational inheritance of adult onset disease in subsequent generations (F1–F3) following ancestral exposure during fetal gonadal sex determination. The current study was designed to determine if a mixture of plastic derived endocrine disruptor compounds bisphenol-A (BPA), bis(2-ethylhexyl)phthalate (DEHP) and dibutyl phthalate (DBP) at two different doses promoted epigenetic transgenerational inheritance of adult onset disease and associated DNA methylation epimutations in sperm. Gestating F0 generation females were exposed to either the “plastics” or “lower dose plastics” mixture during embryonic days 8 to 14 of gonadal sex determination and the incidence of adult onset disease was evaluated in F1 and F3 generation rats. There were significant increases in the incidence of total disease/abnormalities in F1 and F3 generation male and female animals from plastics lineages. Pubertal abnormalities, testis disease, obesity, and ovarian disease (primary ovarian insufficiency and polycystic ovaries) were increased in the F3 generation animals. Kidney and prostate disease were only observed in the direct fetally exposed F1 generation plastic lineage animals. Analysis of the plastics lineage F3 generation sperm epigenome previously identified 197 differential DNA methylation regions (DMR) in gene promoters, termed epimutations. A number of these transgenerational DMR form a unique direct connection gene network and have previously been shown to correlate with the pathologies identified. Observations demonstrate that a mixture of plastic derived compounds, BPA and phthalates, can promote epigenetic transgenerational inheritance of adult onset disease. The sperm DMR provide potential epigenetic biomarkers for transgenerational disease and/or ancestral environmental exposures.
2014-07-22 | GSE59555 | GEO
Project description:The goal of this study was to determine the effects of a well-characterized anti-androgen, abiraterone acetate, and a suspected human anti-androgen, di-n-butyl phthalate (DBP) on the androgenic function of human fetal testis. Human fetal testis was xenografted into the renal subcapsular space of castrated male athymic nude mice. Hosts were treated with hCG to stimulate testosterone production in the xenografts, and were concurrently treated with either abiraterone acetate or DBP. While abiraterone acetate (14 d, 75 mg/kg/d p.o.) dramatically reduced testosterone and the weights of androgen-sensitive host organs, DBP (14 d, 500 mg/kg/d p.o.) had no effect on androgenic endpoints. Three paired analyses were performed using the LIMMA package in R (commands lmfit and eBayes), with the Benjamini-Hochberg correction for multiple comparisons (Smyth 2005): vehicle-treated xenografts vs. unimplanted testis (n=5), abiraterone-treated xenografts vs. matched control xenografts (n=3), and DBP-treated xenografts vs. matched control xenografts (n=3). There were significant differences in gene expression between grafted and ungrafted samples, including dramatic upregulation of microRNAs. Gene expression analysis also showed that abiraterone decreased expression of genes related to cell differentiation, while DBP induced expression of oxidative stress response genes and decreased expression of factors related to embryonic development.
2013-10-31 | GSE49244 | GEO