Inhalation exposure of hexanal in rats (mRNA)
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE60118 | GEO | 2014/08/06
SECONDARY ACCESSION(S): PRJNA257523
REPOSITORIES: GEO
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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 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: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 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:Inhalation exposure of hexanal in rats
| PRJNA257747 | ENA
Project description:Zinc is a common metal in most ambient particulate matter (PM), and has been proposed to be a causative component in PM-induced adverse cardiovascular health effects. Zinc is also an essential metal and has the potential to induce many physiological and nonphysiological changes. Most toxicological studies employ high levels of zinc. We hypothesized that subchronic inhalation of environmentally relevant levels of zinc would cause cardiac changes in healthy rats. To address this question, healthy male WKY rats (12 wks age) were exposed via nose only inhalation to filtered air or 10, 30 or 100 ug/m3 of aerosolized Zn in sulfate form, 5 h/d, 3 d/wk for 16 wks. Necropsies occurred 48 h after the last exposure to ensure effects were due to chronic exposure rather than the last exposure. No significant changes were observed in neutrophil or macrophage count, total lavageable cells, or enzyme activity levels (lactate dehydrogenase, n-acetyl ?-D-glucosaminidase, ?-glutamyl transferase) in bronchoalveolar lavage fluid, indicating minimal pulmonary effect. In the heart, cytosolic glutathione peroxidase activity decreased, while mitochondrial ferritin levels increased and succinate dehydrogenase activity decreased, suggesting a mitochondria-specific effect. Although no cardiac pathology was seen, cardiac gene array analysis indicated changes in genes involved in cell signaling, a pattern concordant with known zinc effects. These data indicate that inhalation of zinc at environmentally relevant levels may induce cardiac effects. While changes are small in healthy rats, these may be especially relevant in individuals with pre-existent cardiovascular disease. Keywords: dose response
2008-09-22 | GSE11091 | GEO
Project description:Open tenotomy of the Achilles tendon of 6 rats was performed. The animals were divided into two groups according to exposure of PM2.5 (particulate matter less than 2.5 µm): control group (Non-PM group) or PM exposure group (PM group). After 6 weeks of PM exposure, the tendon DNA was extracted and anlyzed. Genome-wide DNA methylation profiles were determinen. DNA amplicons were prepared using Differential Methylation Hybridization (DMH) method, subsequently hybridized on to the Customized Agilent Rat CpG island Microarray. The goal was to unravel the DNA methylation patterns in different subgropus of tendon tissue according to partciulate matter exposure.
2022-08-03 | GSE200709 | GEO
Project description:Inhalation exposure of hexanal in rats (DNA methylation)
| PRJNA530909 | 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.
2014-07-01 | GSE49144 | GEO
Project description:Phosphine (PH3) is a highly toxic, corrosive, flammable, heavier-than-air gas that is a commonly used fumigant. Although the mechanism of toxicity is unclear, PH3 is thought to be a metabolic poison. PH3 exposure induces multi-organ toxicity and no effective antidotes or therapeutics have been identified. To better characterize the mechanism(s) driving PH3-induced toxicity we have performed transcriptomic analysis on conscious adult male Sprague-Dawley rats following whole-body inhalation exposure to phosphine gas at three concentrations. PH3 exposure induced concentration- and time-dependent changes in gene expression across multiple tissues.
2020-12-30 | GSE164007 | GEO