Effect of dioxin on maternal rats at postpartum day 7
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PROVIDER: PRJNA560678 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Effect of dioxin on hypothalamic mRNAs in maternal rats at postpartum day 7
| PRJNA560676 | ENA
Project description:Effect of dioxin on pituitary mRNAs in maternal rats at postpartum day 7
| PRJNA560677 | ENA
Project description:We found that oral administration of TCDD (1 µg/kg) to pregnant rats on gestational day 15 suppressed maternal production of prolactin, a pituitary hormone essential for nursing including milk production, during the lactational stage. To comprehensively investigate genes linked to the lower prolactin expression, we performed a DNA microarray analysis in the pituitary of lactating dam rats.
2020-06-19 | GSE135932 | GEO
Project description:We found that oral administration of TCDD (1 µg/kg) to pregnant rats on gestational day 15 suppressed maternal production of prolactin, a pituitary hormone essential for nursing including milk production, during the lactational stage. To comprehensively investigate genes linked to the lower prolactin expression, we performed a DNA microarray analysis in the hypothalamus, which regulates the pituitary prolactin synthesis, of lactating dam rats.
2020-06-19 | GSE135931 | GEO
Project description:Effect of maternal dioxin exposure on pituitary mRNAs in fetal rats at gestational day 18
| PRJNA576836 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2020-06-20 | GSE135933 | GEO
Project description:The dioxin congener 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) causes a wide range of toxic effects in rodent species, all of which are mediated by a ligand-dependent transcription-factor, the aryl hydrocarbon receptor (AHR). The Han/Wistar (Kuopio) (H/W) strain shows exceptional resistance to many TCDD-induced toxicities; the LD50 of >9600 µg/kg for H/W rats is higher than for any other wild-type mammal known. We have previously shown that this resistance primarily results from H/W rats expressing a variant AHR isoform that has a substantial portion of the AHR transactivation domain deleted. Despite this large deletion, H/W rats are not entirely refractory to the effects of TCDD; the variant AHR in these animals remains fully competent to up-regulate well-known dioxin-inducible genes. TCDD-sensitive (Long-Evans, L-E) and resistant (H/W) rats were treated with either corn-oil (with or without feed-restriction) or 100 µg/kg TCDD for either four or ten days. Hepatic transcriptional profiling was done using microarrays, and was validated by RT-PCR analysis of 41 genes. . A core set of genes was altered in both strains at all time points tested, including CYP1A1, CYP1A2, CYP1B1, Nqo1, Aldh3a1, Tiparp, Exoc3, and Inmt. Outside this core, the strains differed significantly in the breadth of response: three-fold more genes were altered in L-E than H/W rats. At ten days almost all expressed genes were dysregulated in L-E rats, likely reflecting emerging toxic responses. Far fewer genes were affected by feed-restriction, suggesting that only a minority of the TCDD-induced changes are secondary to the wasting syndrome.
2011-11-14 | GSE13513 | GEO
Project description:We found that oral administration of TCDD (1 µg/kg) to pregnant rats on gestational day 15 suppressed pituitary syntheisis of growth hormone during the last fetal stage. We performed a DNA microarray analysis to identify the genes linked to the attenuated expression of GH, using the male and female fetal pituitary at GD18 when the reduced expression of GH started to occur because of TCDD.
2021-01-29 | GSE138694 | GEO
Project description:Our previous studies have revealed that treatment of pregnant rats with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, 1 μg/kg) at gestational day (GD) 15 reduces the pituitary synthesis of luteinizing hormone (LH) during late fetal and early postnatal period, leading to imprinting of defects in sexual behaviors at adulthood. However, it remains obscure how the attenuation of pituitary LH links to sexual immaturity. To address this issue, we firstly performed a DNA microarray analysis to identify the gene(s) responsible for dioxin-induced sexual immaturity, using the pituitary and hypothalamus of male pups, at the age of postnatal day (PND)70, born from TCDD-treated dams. Among the reduced genes, we focused on gonadotropin-releasing hormone (GnRH) in the hypothalamus, because of its role in sexual behaviors suggested so far. The present study strongly suggests that maternal exposure to TCDD fixes the status of the lowered expression of GnRH in the offspring by reducing steroidogenesis at perinatal stage, and this is the mechanism for the imprinting of defects in sexual behaviors at adulthood.
2013-08-21 | GSE48100 | GEO
Project description:The dioxin congener 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) causes a wide range of toxic effects in rodent species, all of which are mediated by a ligand-dependent transcription-factor, the aryl hydrocarbon receptor (AHR). The Han/Wistar (Kuopio) (H/W) strain shows exceptional resistance to many TCDD-induced toxicities; the LD50 of >9600 µg/kg for H/W rats is higher than for any other wild-type mammal known. We have previously shown that this resistance primarily results from H/W rats expressing a variant AHR isoform that has a substantial portion of the AHR transactivation domain deleted. Despite this large deletion, H/W rats are not entirely refractory to the effects of TCDD; the variant AHR in these animals remains fully competent to up-regulate well-known dioxin-inducible genes. TCDD-sensitive (Long-Evans, L-E) and resistant (H/W) rats were treated with either corn-oil (with or without feed-restriction) or 100 µg/kg TCDD for either four or ten days. Hepatic transcriptional profiling was done using microarrays, and was validated by RT-PCR analysis of 41 genes. . A core set of genes was altered in both strains at all time points tested, including CYP1A1, CYP1A2, CYP1B1, Nqo1, Aldh3a1, Tiparp, Exoc3, and Inmt. Outside this core, the strains differed significantly in the breadth of response: three-fold more genes were altered in L-E than H/W rats. At ten days almost all expressed genes were dysregulated in L-E rats, likely reflecting emerging toxic responses. Far fewer genes were affected by feed-restriction, suggesting that only a minority of the TCDD-induced changes are secondary to the wasting syndrome. Rats from sensitive (Long-Evans, LE) and resistant (Han/Wistar, HW) strains were treated with 100 ug/kg TCDD or corn oil vehicle and sacrificed either 4 or 10 days after treatment. LE control rats were either fed normally or feed-restricted to control for the wasting effects of TCDD treatment. Each treatment group contains four or five animals (biological replicates), each of which was assayed on an individual microarray.
2011-11-14 | E-GEOD-13513 | biostudies-arrayexpress