Inhalation exposure of hexanal in rats (DNA methylation)
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PROVIDER: PRJNA530909 | ENA |
REPOSITORIES: ENA
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Project description:Inhalation exposure of hexanal in rats
| PRJNA257747 | ENA
Project description:To further development of insight into the mechanism of toxicity, it is important to employ whole genome microarray expression profiling to identify and characterize DNA methylation profiles as a discovery platform relevant for toxicologic mechanisms of hexanal. DNA methylation have prominent epigenetic role in regulation of gene expression, cell cycle control, apoptosis, cancer development and proliferation-related processes. However, few reports have described the effect of hexanal on DNA methylation expression profiles using animal model. In this respect, we studied the expression profiles of DNA methylation in hexanal-exposed in rats by DNA methylation microarray analysis.
2019-04-05 | GSE129313 | GEO
Project description:To further development of insight into the mechanism of toxicity, it is important to employ whole genome microarray expression profiling as a discovery platform to ientify genes with the potential to distinguish hexanal exposure across an exposure range relevant for toxicologic mechanisms. However, few reports have described the effect of hexanal on gene expression profiles using animal model. In this respect, we studied the expression profiles of mRNAs in hexanal-exposed in rats by microarray analysis. To evaluate the gene expression in lung tissue of rats after exposure of hexanal, Fischer-344 rats were inhaled to three concentrations (600, 1000, 1500 mg/m3) for 5 weeks. mRNA expression analysis was conducted using Rat GE(v3) 4X44K microarray (Agilent Technologies, USA).
2014-08-06 | E-GEOD-60118 | biostudies-arrayexpress
Project description:To further development of insight into the mechanism of toxicity, it is important to employ whole genome microarray expression profiling as a discovery platform to ientify genes with the potential to distinguish hexanal exposure across an exposure range relevant for toxicologic mechanisms. However, few reports have described the effect of hexanal on gene expression profiles using animal model. In this respect, we studied the expression profiles of mRNAs in hexanal-exposed in rats by microarray analysis.
2014-08-06 | GSE60118 | GEO
Project description:To further development of insight into the mechanism of toxicity, it is important to employ whole genome microarray expression profiling to identify and characterize miRNAs profiles as a discovery platform relevant for toxicologic mechanisms of hexanal. miRNAs have prominent role in cell cycle control, apoptosis, cancer development and proliferation-related processes. However, few reports have described the effect of hexanal on miRNA expression profiles using animal model. In this respect, we studied the expression profiles of miRNAs in hexanal-exposed in rats by miRNA microarray analysis. To evaluate the miRNA expression in lung tissue of rats after exposure of hexanal, Fischer-344 rats were inhaled to three concentrations (600, 1000, 1500 mg/m3) for 5 weeks. miRNA expression analysis was conducted using Rat miRNA 8 x 15K microarray v19.0 (Agilent Technologies, USA).
2014-08-08 | E-GEOD-60203 | biostudies-arrayexpress
Project description:To further development of insight into the mechanism of toxicity, it is important to employ whole genome microarray expression profiling to identify and characterize miRNAs profiles as a discovery platform relevant for toxicologic mechanisms of hexanal. miRNAs have prominent role in cell cycle control, apoptosis, cancer development and proliferation-related processes. However, few reports have described the effect of hexanal on miRNA expression profiles using animal model. In this respect, we studied the expression profiles of miRNAs in hexanal-exposed in rats by miRNA microarray analysis.
2014-08-08 | GSE60203 | GEO
Project description:Inhalation exposure of hexanal in rats (miRNA)
| PRJNA257748 | ENA
Project description:Inhalation exposure of hexanal in rats (mRNA)
| PRJNA257523 | ENA
Project description:Occupational exposure to crystalline silica results in serious health effects, most notably, silicosis and cancer. A proper understanding of the mechanism(s) underlying the initiation and progression of silica-induced pulmonary toxicity is critical for the intervention and/or prevention of the adverse health effects associated with crystalline silica exposure. Rats were exposed to crystalline silica by inhalation at a concentration of 15 mg/m3, 6 hours/day, 5 days/week for 3, 6 or 12 weeks. At the end of each exposure time point, toxicity and global gene expression changes were determined in the lungs. In general, silica exposure resulted in pulmonary toxicity that was dependent on the duration of silica exposure. A significant and silica exposure time-dependent increase in lactate dehydrogenase activity and accumulation of alveolar macrophages and infiltrating neutrophils in the bronchoalveolar lavage fluid suggested crystalline silica-induced pulmonary toxicity in the rats. Histological changes indicative of pulmonary toxicity were detectable only in the lungs of rats that were exposed to silica for 6- or 12-weeks. Minimal, sub-acute pulmonary inflammation consisting mainly of macrophage accumulation and infiltration of neutrophils was seen in 2 out of 8 rats in the 6-week silica exposure group. Chronic active inflammation, type II pneumocyte hyperplasia, and fibrosis were detected following 12-weeks of silica exposure in all rat lungs. In addition, crystalline silica was visible in the lungs of the rats belonging to the 12-week exposure group. A significant increase in the number of neutrophils seen in the blood indicated silica-induced systemic inflammation in the rats. Microarray analysis of the global gene expression profiles of the rat lungs detected significant differential expression (FDR p <0.05 and fold change >1.5) of 38, 77 and 99 genes in the rats exposed to silica for 3-, 6- and 12-weeks, respectively, compared to the time-matched controls. Bioinformatics analysis of the differentially expressed genes identified significant enrichment of functions, networks and pathways related to inflammation, cancer, oxidative stress, fibrosis and tissue remodeling in the lungs of the silica exposed rats. Collectively, the results of our study provided insights into the molecular mechanisms underlying pulmonary toxicity following sub-chronic exposure to silica in rats. 36 samples were analyzed in this experiment. 6 rats were exposed to crystalline silica by inhalation 15 mg/m3, 6 hours/day, 5 days, 3 weeks. 6 rats were exposed to crystalline silica by inhalation 15 mg/m3, 6 hours/day, 5 days, 6 weeks. 6 rats were exposed to crystalline silica by inhalation 15 mg/m3, 6 hours/day, 5 days, 12 weeks. 18 rats served as controls (6 for each 3 week, 6 week, and 12 week exposure) and were exposed to air during treatment times. Lung gene expression profiling was performed using RNA isolated from rat lung samples.
2014-07-01 | E-GEOD-49144 | biostudies-arrayexpress
Project description:The lung response to inhalation exposure to oil vapor particles was investigated in a rat model. Adult male Sprague-Dawley rats were exposed by whole-body inhalation to air or an aerosol containing oil vapor particles at concentrations of 300 ppm, 6 hours/day for 1 day (shot-term) or 300 ppm, 6 hours/day, 4 days/week for 4 weeks (long-term). The control and oil vapor exposed rats were euthanized at post-exposure time intervals of 1 and 28 days and lung toxicity determined. Analysis of bronchoalveolar lavage parameters of toxicity such as lactate dehydrogenase activity, oxidant generation, and inflammation did not reveal any significant lung toxicity in the oil vapor exposed rats. Approximately 50 genes each were found significantly differentially expressed in both the short- and long-term exposure groups of the rats at the one-day post-exposure time interval. The data obtained from the present study demonstrated that oil vapor inhalation exposure, under the exposure conditions employed in the present study, did not result in any significant lung toxicity in the rats despite the gene expression changes detected.
2022-12-31 | GSE152187 | GEO