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
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.
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.
Project description:Our project focuses on the effects of an in utero TCDD exposure on the male reproductive function. Keywords: transcriptionnal analysis
Project description:Our project focuses on the effects of an in utero TCDD exposure on the male reproductive function. Keywords: transcriptionnal analysis
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.
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
Project description:Bisphenol-A is a widespread endocrine disruptor chemical. In utero or perinatal exposure to bisphenol-A (BPA), leads to impaired glucose metabolism during adulthood. To investigate the consequences of the exposure to bisphenol-A during development in pancreatic beta-cell growth We used microarrays to determine gene expression changes resulting from exposure to bisphenol-A during pregnancy in pancreatic islets of the male offspring at postnatal day 30.
