Consequences of an in utero TCDD exposure on the male reproductive function in 5 postnatal days rat
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE13812 | GEO | 2010/12/01
SECONDARY ACCESSION(S): PRJNA114597
REPOSITORIES: GEO
Similar Datasets
Project description:Our project focuses on the effects of an in utero TCDD exposure on the male reproductive function. Keywords: transcriptionnal analysis
2010-12-01 | GSE13838 | GEO
Project description:Our project focuses on the effects of an in utero TCDD exposure on the male reproductive function. Keywords: transcriptionnal analysis Pregnant rats were given either one oral dose of 2,3-7,8 TCDD (200 ng/kg) or equal volume of vehicule (sesame oil). Male rats were sacrified 28 postnatal days and testes were harvested. RNA were extracted with Rneasy mini kit. A pool of RNA from vehicule group was used as the reference group. Each rat submitted to TCDD was compared to reference group. Four biological replicates were processed in a dye swap experimental plan.
2010-12-01 | E-GEOD-13838 | biostudies-arrayexpress
Project description:Our project focuses on the effects of an in utero TCDD exposure on the male reproductive function. Keywords: transcriptionnal analysis Pregnant rats were given either one oral dose of 2,3-7,8 TCDD (200 ng/kg) or equal volume of vehicule (sesame oil). Male rats were sacrified 5 postnatal days and testes were harvested. RNA were extracted with Rneasy mini kit. A pool of RNA from vehicule group was used as the reference group. Each rat submitted to TCDD was compared to reference group. Four biological replicates were processed in a dye swap experimental plan.
2010-12-01 | E-GEOD-13812 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE13812: Consequences of an in utero TCDD exposure on the male reproductive function in 5 postnatal days rat GSE13838: Consequences of an in utero TCDD exposure on the male reproductive function in 28 postnatal days rat Refer to individual Series
2010-12-01 | E-GEOD-13839 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the SubSeries listed below.
2010-12-01 | GSE13839 | GEO
Project description:[Original title] In utero and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induces disruption of the prostate glands and fibrosis in rhesus monkeys. We investigated the effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure on the prostate in rhesus monkey offspring. Dams received 0, 30 or 300 ng/kg TCDD subcutaneously on Day 20 of gestation, and then 5% of the initial dose was injected every 30 days until Day 90 after delivery. The offspring were maintained until reaching sexual maturity, and examined histopathologically. Dose-dependent decreases in the prostate glands and widespread fibrosis were observed in offspring. It is noteworthy that 7 years from the final lactational TCDD exposure, inflammatory cell infiltration and disruption of the prostate glands were also observed. Differential mRNA expression associated with fibrosis, inflammatory response and disruption of cell components were demonstrated by microarray analysis, and up-regulation of TGM4, TGFB1, COL1A1 and MMP2 was confirmed with Real-time PCR. In conclusion, in utero and lactational exposure to TCDD induced dose-proportional prostatic fibrosis, indicating prostatic dysfunction and inducible semen quality reduction in second-generation rhesus monkeys.
2010-01-28 | GSE20043 | GEO
Project description:[Original title] In utero and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induces disruption of the prostate glands and fibrosis in rhesus monkeys. We investigated the effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure on the prostate in rhesus monkey offspring. Dams received 0, 30 or 300 ng/kg TCDD subcutaneously on Day 20 of gestation, and then 5% of the initial dose was injected every 30 days until Day 90 after delivery. The offspring were maintained until reaching sexual maturity, and examined histopathologically. Dose-dependent decreases in the prostate glands and widespread fibrosis were observed in offspring. It is noteworthy that 7 years from the final lactational TCDD exposure, inflammatory cell infiltration and disruption of the prostate glands were also observed. Differential mRNA expression associated with fibrosis, inflammatory response and disruption of cell components were demonstrated by microarray analysis, and up-regulation of TGM4, TGFB1, COL1A1 and MMP2 was confirmed with Real-time PCR. In conclusion, in utero and lactational exposure to TCDD induced dose-proportional prostatic fibrosis, indicating prostatic dysfunction and inducible semen quality reduction in second-generation rhesus monkeys. Dam received 0, 30 or 300 ng/kg TCDD subcutaneously on Day 20 of gestation, and then 5% of the initial dose was injected every 30 days until Day 90 after delivery. The offspring were maintained until reaching sexual maturity, and the prostates from 3 offspring in each group were evalutated by histopathological examination, microarray analysis and Real-time quantitative PCR. Supplementary file: Fold_change comparison results of 'control group vs 30 ng/kg group' and 'control group vs 300 ng/kg group'.
2010-01-27 | E-GEOD-20043 | biostudies-arrayexpress
Project description:We report the RNAseq-based transcriptome profiles of rat gestation day 20 dam liver, fetal male and female liver, fetal male pituitary, and fetal testis following in utero exposure to either 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or 2,3,7,8-tetrachlorodibenzofuran (TCDF). Two exposure models were examined: 1) pregnant rats exposed to either a dose response series of TCDD or TCDF from gestation day 6 - 20 or 2) pregnant rats exposed to a single dose of TCDD or TCDF on gestation day 15. These data support a mode-of-action for dioxin-induced rat male reproductive toxicity involving key events in both the fetal pituitary (reduced gonadotropin production) and fetal testis (reduced Leydig cell cholesterologenesis and steroidogenesis) which are hypothesized to decrease perinatal Sertoli cell proliferation and culminate in reduced spermatogenesis. The lack of a TCDF effect on proposed key events may be due to a higher rate of metabolic clearance relative to TCDD.
2019-12-15 | GSE128824 | GEO
Project description:Targeted proteomics using an inclusion list in a data-dependent acquisition method. Mouse prostates were analyzed to determine the effects of developmental exposure to the dioxin TCDD after hormone treatment
2020-03-30 | PXD014752 | Pride
Project description:2,3,7,8-TCDD (TCDD) is a reproductive toxicant and endocrine disruptor in nearly all vertebrates, yet the mechanisms by which TCDD induces these reproductive alterations have not been fully characterized. Fish are among the most sensitive vertebrates to the toxic effects of TCDD, and even subtle physiologic changes induced by TCDD can impair reproduction. Previously, we have shown that chronic, sub-lethal exposure to TCDD decreased reproductive capacity, reduced serum estradiol and vitellogenin concentrations, and altered follicular development. Here we investigate the transcriptional changes in zebrafish ovary as they relate to observed attenuated estradiol concentrations and ovarian development. We used quantitative RT-PCR to assess TCDDâs effects on the expression of several candidate genes important in the regulation of follicular development and steroidogenesis. Additionally, global changes in gene expression in the ovary caused by TCDD exposure were identified using Affymetrix Gene Chip Analysis. Our data suggest that TCDD may inhibit follicle maturation via attenuated gonadotropin responsiveness and/or depressed estradiol biosynthesis. Additionally, genes involved in glucose and lipid metabolism, regulation of transcription, and immune function were dysregulated by at least 2-fold suggesting that TCDD alters various integrated networks of signaling pathways. Approximately 89% of dysregulated transcripts contain putative AHR response elements (AHRE) within 5kb upstream of the predicted transcriptional start site suggesting ovarian toxicity is AHRE driven. Furthermore, approximately 49% of dysregulated transcripts contain putative estrogen response elements (ERE) suggesting that dysregulation of estrogen-responsive genes may also contribute to TCDD-induced attenuated follicular development. Patterns in gene expression were correlated with putative EREs and AHREs, and suggest that impacts on the regulation of transcription may play a large role in TCDDâs ovarian toxicity. Taken together, these data illustrate the complexity of TCDDâs ovarian toxicity. Experiment Overall Design: A total of eight samples were analyzed including three TCDD doses (10, 40, 100 ppb, dietary exposure) and vehicle control samples. cRNA targets were synthesized from pooled total RNA isolated from five ovaries from different individuals in each treatment group. Each individual contributed equally to a given pool. Two technical replicates were run for each treatment group. Several genes of interest arising from this microarray study were validated by Quantitative RT-PCR with individual ovary samples to assess biological variability.
2009-04-30 | E-GEOD-4859 | biostudies-arrayexpress