Rattus norvegicus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA140557 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Synergism of Iraqi Sand/Cigarette Smoke Co-Exposure in Rats. 24 samples are used.
2012-01-01 | GSE28804 | GEO
Project description:Synergism of Iraqi Sand/Cigarette Smoke Co-Exposure in Rats. 24 samples are used. A total of 102 rats will be separated into six exposure groups: each group consisting of 17 male CD Sprague-Dawley rats, 10 to 15 weeks old. The six exposure groups were each exposed via two routes: 1. nose-only inhalation exposures --- air or cigarette smoke; 2. whole-body inhalation exposures -- air or manufactured silica sand or Iraqi sand. The nose only exposures were conducted 3 hours per day, 5 days per week for 6 weeks. During the last two weeks of the nose - only exposures, whole-body exposure were also conducted 18-19 hours per day, 7 days per week.
2012-01-01 | E-GEOD-28804 | biostudies-arrayexpress
Project description:Gene expression profiles in lung tissue of rats following exposure to mainstream cigarette smoke
| PRJNA94523 | ENA
Project description:Previous studies have shown that smoking induces oxidative stress and inflammation, known factors that coincide with the development and progression of silicosis. Nevertheless, the precise role of cigarette smoke exposure in silicosis and the underlying mechanisms are not clearly understood. Therefore, the objective of the present study was to determine the effect of smoking, if any, on silica-induced pulmonary response and the underlying mechanisms. Pulmonary toxicity and lung gene expression profiles were determined in male Fischer 344 rats exposed to air, crystalline silica, cigarette smoke or cigarette smoke plus crystalline silica. Silica exposure resulted in significant pulmonary toxicity which was further exacerbated by cigarette smoke exposure in the rats. Significant differences in the gene expression profiles were detected in the lungs of the rats exposed to cigarette smoke, silica or a combination of both compared with the control rats.
2020-11-01 | GSE136945 | GEO
Project description:low and high aerobic capacity rats exposed to cigarette smoke, lung tissue
| PRJNA128635 | ENA
Project description:Our previous studies have shown that tobacco smoke exposure exacerbated the lung response to crystalline silica exposure in rats. The objective of the present study, a follow-up to our previous study, was to determine the effect of tobacco smoke exposure cessation on the lung response to crystalline silica exposure in the rats. Rats were exposed to air, crystalline silica (1 week followed by a 1 year progression/recovery period with no exposure), tobacco smoke (6 months of exposure followed by 6 months of recovery with no exposure), or crystalline silica (1 week) plus tobacco smoke (6 months of exposure followed by 6 months of recovery with no exposure). Lung toxicity was determined at the end of the 1-year progression/recovery period in all 4 groups of the rats. Silica exposure resulted in significant lung toxicity which was further exacerbated by tobacco smoke exposure in the rats. Cessation of cigarette smoke exposure did not result in reversal of the silica-induced lung toxicity despite exacerbation of the toxicity by tobacco smoke.
2024-12-31 | GSE155924 | GEO
Project description:Modifications of the Rat Airway Explant Transcriptome by Cigarette Smoke
| PRJNA115657 | ENA
Project description:The kinetics of transcriptomic changes induced by cigarette smoke in rat lungs
| PRJNA95279 | ENA
Project description:Cigarette smoking remains the leading cause of non-small cell lung carcinoma. Studies involving acute exposure of smoke on lung cells revealed induction of pre- cancerous state in lung cells. Recently few studies have reported the chronic effect of cigarette smoke in inducing cellular transformation. Yet no systemic study has been performed to understand the molecular alterations in lung cells due to cigarette smoke. Hence it is both important and necessary to study the chronic effect of cigarette smoke in a temporal setting to understand the molecular alterations. In this study, we carried out TMT based proteomic profiling of lung cells which were exposed to cigarette smoke condensate (CSC) for upto 12 months. We identified 2621 proteins in total, of which 145, 114, 87, 169 and 671 proteins were differentially expressed (p<0.05, 1.5 fold) in 2nd, 4th, 6th, 8th and 12th month respectively. Pathway analysis revealed enrichment of xenobiotic metabolism signaling for the first 8 months of smoke treatment, where as continued exposure of smoke for 12 months revealed mitochondrial reprogramming in cells which includes dysregulation of oxidative phosphorylation machinery leading to enhanced reactive oxygen species and higher expression of enzymes involved in tricarboxylic acid cycle (TCA). In addition, chronic exposure of smoke led to overexpression of enzymes involved in glutamine metabolism, fatty acid degradation and lactate synthesis. This could possibly explain the availability of alternative source of carbon in TCA cycle apart from glycolytic pyruvate. Our data indicates that chronic exposure to cigarette smoke induces mitochondrial metabolic transformation in cells to support growth and survival.
2022-03-02 | PXD007108 | Pride