Rattus norvegicus
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ABSTRACT:
PROVIDER: PRJNA276308 | ENA |
REPOSITORIES: ENA
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Project description:With the advent of high information content technologies, especially microarrays, it is pertinent to determine the impact of molecular data on the NOAELs. Consequently, we conducted an integrative study to identify a no transcriptomic effect dose using microarray analyses coupled with qPCR and determined how this correlated with the NOAEL. We assessed the testicular effects of the antiandrogen, flutamide (FM), in a rat 28-day toxicity study using doses of 0.2-30 mg/kg/day. Concerning molecular data, we observed differential gene expression starting from 1 mg/kg/day and a deregulation of more than 1500 genes at 30 mg/kg/day. Dose-related changes were identified for the major pathways associated with the testicular lesion (eg fatty acid metabolism), that were confirmed by qPCR. These data, along with standard measurements supported the no effect dose of 0.2 mg/kg/day.
2011-03-29 | GSE28202 | GEO
Project description:Male Sprague-Dawley rats [Crl:CD®(SD)IGS BR], weighing ~250 g at study initiation were obtained from Charles River Laboratories, Inc. (Wilmington, MA). Rats were housed singly in ventilated, stainless steel, wire-bottom hanging cages and fed non-certified Rodent Chow (Harlan Labs, Madison, WI) and water ad libitum and acclimated for at least 5 days after arrival. Rats were randomly assigned to various treatment groups (3 rats/group) and were dosed once daily by oral gavage with vehicle (0.2% hydroxypropylmethylcellulose at a dose volume of 10 ml/kg) or with 30, 100, or 200 mg/kg of A-998679. All rats were fasted overnight after their last dose, weighed and sacrificed under isoflurane anesthesia. Liver and small intestine (jejunum) were flash frozen in liquid nitrogen and stored at −80°C until processing for gene expression profiling on the Affymetrix platform.
2012-08-04 | GSE39850 | GEO
Project description:Male Sprague-Dawley rats [Crl:CD®(SD)IGS BR], weighing ~250 g at study initiation were obtained from Charles River Laboratories, Inc. (Wilmington, MA). Rats were housed singly in ventilated, stainless steel, wire-bottom hanging cages and fed non-certified Rodent Chow (Harlan Labs, Madison, WI) and water ad libitum and acclimated for at least 5 days after arrival. Rats were randomly assigned to various treatment groups (3 rats/group) and were dosed once daily by oral gavage with vehicle (0.2% hydroxypropylmethylcellulose at a dose volume of 10 ml/kg) or with 30, 100, or 200 mg/kg of A-998679. All rats were fasted overnight after their last dose, weighed and sacrificed under isoflurane anesthesia. Liver and small intestine (jejunum) were flash frozen in liquid nitrogen and stored at −80°C until processing for gene expression profiling on the Affymetrix platform.
2012-07-24 | GSE39525 | GEO
Project description:Male Sprague-Dawley rats were given NOS inhibitor L-NNA (500 mg/l water) for 4 days, 21 days or 21 days with Vitamin E in chow (0.7 g/kg BW/day) (4d-LNNA, 21d-LNNA and 21d-LNNA+VitE, respectively).
2007-03-01 | E-UMCU-18 | biostudies-arrayexpress
Project description:With the advent of high information content technologies, especially microarrays, it is pertinent to determine the impact of molecular data on the NOAELs. Consequently, we conducted an integrative study to identify a no transcriptomic effect dose using microarray analyses coupled with qPCR and determined how this correlated with the NOAEL. We assessed the testicular effects of the antiandrogen, flutamide (FM), in a rat 28-day toxicity study using doses of 0.2-30 mg/kg/day. Concerning molecular data, we observed differential gene expression starting from 1 mg/kg/day and a deregulation of more than 1500 genes at 30 mg/kg/day. Dose-related changes were identified for the major pathways associated with the testicular lesion (eg fatty acid metabolism), that were confirmed by qPCR. These data, along with standard measurements supported the no effect dose of 0.2 mg/kg/day. Flutamide was administered in suspension to rats (7 weeks old at start of treatment, 10 per group) by oral gavage at a daily dose of 0 (control), 0.2, 1, 6 and 30 mg/kg body weight, for 28 consecutive days. Dose-related changes in gene expression were determined in the testes using whole genome oligonucleotide microarrays.
2011-03-29 | E-GEOD-28202 | biostudies-arrayexpress
Project description:Rodent studies have indicated that gestational and perinatal bisphenol A (BPA) exposure increase the risk of developing breast cancer during adulthood. In contrast, some dietary compounds such as genistein (GEN) and indole 3-carbinol (I3C) present potential protective effects against inducing hormone-dependent cancers, including that of the mammary gland. Thus, we aimed to evaluate the role of these dietary compounds on early mammary gland development and carcinogenesis in female Sprague-Dawley offspring. Pregnant Sprague-Dawley (SD) rats were treated with BPA at 25 or 250µg/kg b.w./day by gavage from gestational day (GD) 10 to 21 with or without dietary GEN (250 mg/kg chow, ~5.5 mg/kg b.w./day) or I3C (2000 mg/kg chow, ~45.0 mg/kg b.w./day). At post-natal day (PND) 21, some female offspring from different litters were euthanized for mammary gland development and gene expression analyses while other female offspring received a single dose of N-methyl-N-nitrosourea (MNU) for mammary carcinogenesis initiation. The findings this study indicated the prenatal exposure to BPA, GEN and I3C did not significantly alter ductal elongation, number of terminal end buds (TEB) or cell proliferation, and estrogen receptor alpha (ER-α) immunostaining expression in epithelial mammary cells at PND 21. BPA treatment modulated the expression of several genes, but these changes were not associated with a dose dependent response. Dietary GEN and I3C treatment causally and consistent with the mammary gland structures outcomes. Besides, maternal BPA exposure associated with dietary GEN and I3C did not alter the susceptibility to the mammary cancer development in adulthood when the carcinogen was administered in a window of immature mammary gland development.
2016-06-03 | GSE68973 | GEO
Project description:In this dose series pregnant CD-1 (outbred) dams were exposed to methylmercury (MeHg) as monomethylmercuric chloride injected intraperitoneally on 9 d.p.c. Test doses were 10.0 mg/kg and below. This regimen induces symptoms of Fetal Minimata Disease (FMD) in term fetuses. Risks with respect to FMD for the various test doses were 10.0 mg/kg (40% risk), 5.0 mg/kg (20% risk), 2.5 mg/kg (NOAEL), and 1.25 mg/kg (subNOAEL). All measurements were on RNA from the embryonic forebrain (prosencephalon and surrounding tissue) at 3.0h post-treatment. Keywords = dose series Keywords = mercury Keywords = embryo Keywords = Fetal Minamata Disease Keywords: dose response
2004-03-11 | GSE1075 | GEO
Project description:Small molecules, BIO and Lithium chloride are widely used to activate Wnt signaling. It has been shown that these molecules induced beta-catenin accumulation and translocation, leading to the activation of Wnt signaling. These molecules also control various cell responses. Here, the differential gene expression of human dental pulp stem cells treated with BIO and Lithium chloride was examined using a high throughput RNA sequencing technique. Results demonstrated that BIO and Lithium chloride regulated the mRNA expression of various genes in human dental pulp stem cells.
2022-08-17 | GSE183633 | GEO
Project description:Nafion byproduct 2 (NBP2; CAS: 749836-20-2; Product #: 6164-3-3J; Lot: 512400; SynQuest Laboratories Alachua, FL, USA) is a polyfluoroalkyl ether sulfonic acid that was recently detected in surface water, drinking water, and human serum samples from monitoring studies in North Carolina, USA. We orally exposed pregnant Sprague-Dawley rats to NBP2 from gestation day (GD) 14–18 (0.1–30 mg/kg/d), GD17-21, and GD8 to postnatal day (PND) 2 (0.3–30 mg/kg/d) to characterize maternal, fetal, and postnatal effects. GD14-18 exposures were also conducted with perfluorooctane sulfonate (PFOS) for comparison to NBP2, as well as data previously published for hexafluoropropylene oxide-dimer acid (HFPO-DA or GenX). NBP2 produced stillbirth (30 mg/kg), reduced pup survival shortly after birth (10 mg/kg), and reduced pup body weight (10 mg/kg). Histopathological evaluation identified reduced glycogen stores in newborn pup livers and hepatocyte hypertrophy in maternal livers at ≥ 10 mg/kg. Exposure to NBP2 from GD14-18 reduced maternal serum total T3 and cholesterol concentrations (30 mg/kg). Maternal, fetal, and neonatal liver gene expression was investigated using RT-qPCR pathway arrays, while maternal and fetal livers were also analyzed using TempO-Seq transcriptomic profiling. Overall, there was limited alteration of genes in maternal or F1 livers from NBP2 exposure with significant changes mostly occurring in the top dose group (30 mg/kg) associated with lipid and carbohydrate metabolism. Metabolomic profiling indicated elevated maternal bile acids for NBP2, but not HFPO-DA or PFOS, while all three reduced 3-indolepropionic acid. Maternal and fetal serum and liver NBP2 concentrations were similar to PFOS, but ∼10–30-fold greater than HFPO-DA concentrations at a given maternal oral dose. NBP2 is a developmental toxicant in the rat, producing neonatal mortality, reduced pup body weight, reduced pup liver glycogen, reduced maternal thyroid hormones, and altered maternal and offspring lipid and carbohydrate metabolism similar to other studied PFAS, with oral toxicity for pup loss that is slightly less potent than PFOS but more potent than HFPO-DA.
2022-01-10 | GSE192589 | GEO
Project description:17alpha-ethinylestradiol (EE2) is one of the most potent estrogens that have the ability to interfere with the endocrine system of fish. The objective was to investigate the effects and mechanisms of action caused by 60 days of dietary exposure to 0.2 mg EE2/kg and 0.07 mg EE2/kg feed in female largemouth bass (LMB) during the reproductive season. Microarrays and pathway analyses were performed on hepatic tissues to identify genes and biological processes altered in female LMB by EE2 exposure. The hypothesis was that the two concentrations of EE2 would produce dose-response changes in sensitive genes. Body and ovary weights were measured and blood was collected for measurement of plasma steroid hormones (17beta-estradiol (E2), testosterone (T)) and vitellogenin (VTG) using ELISA. The 0.2 mg EE2/kg feed exposure reduced the gonadosomatic index (GSI) by 75%, and plasma levels of E2 and T were reduced by over 90%. Plasma VTG was increased by approximately 100% (from 4 to 8mg/ml) by the 0.2 mg/kg treatment. T levels, from the 0.07 mg EE2/kg feed, reduced GSI by approximately 30% and circulating E2 and T by ~80% but did not affect VTG concentrations. We found 1,594 and 1,165 genes were significantly affected (p<0.05) by the 0.07 mg EE2/kg feed and 0.2 mg EE2/kg feed, respectively. Gene ontology (GO) analysis revealed that there were different biological processes regulated by the two concentrations of EE2. Pathway analysis showed that the 0.07 mg EE2/kg feed exposure caused differential regulation of genes associated with fatty acid biosynthesis and glycolysis, indicating some metabolic effects. In contrast, the 0.2 mg EE2/kg feed exposure altered transcription of genes involved in immune response and apoptosis, suggesting a toxic response at this concentration. These results suggest that the two concentrations demonstrated distinct physiological responses, with the higher concentration inducing complete endocrine disruption in LMB. These findings demonstrate the usefulness of microarrays to identify possible biomarkers and modes of toxic action to dietary exposure in LMB. Two concentrations of EE2 would produce dose-response changes in sensitive genes. Female LMB were fed 5 days per week for 60 days with floating pellets that contained 0.07 or 0.2 mg/kg of EE2.
2011-03-24 | E-GEOD-28143 | biostudies-arrayexpress