Pulmonary effects of inhaled diesel exhaust and fracking sand particles in rats
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PROVIDER: PRJNA1011879 | ENA |
REPOSITORIES: ENA
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Project description:The pulmonary response to inhalation exposure to diesel exhaust particles (DEP) and fracking sand particles (FSD) was investigated in a rat model. Healthy adult male Sprague-Dawley rats were exposed by whole-body inhalation to air (control) or an aerosol containing DEP at a concentration of 1.0 mg/m3 combined with FSD at concentrations of 30 mg/m3, 6 hours/day for 4 days. The control and DEP/FSD exposed rats were euthanized at post-exposure time intervals of 1, 7, or 27 days and pulmonary inflammatory, cytotoxic, and oxidant responses were determined. Analysis of bronchoalveolar lavage parameters of toxicity such as lactate dehydrogenase activity, oxidant generation, and inflammation revealed only minimal changes in pulmonary toxicity in the DEP/FSD-exposed rats, compared with the time-matched controls. The lung gene expression profiles showed only minimal changes in the DEP/FSD exposed rats compared with the controls. Specifically, there were a total of 6 genes significantly differentially expressed (fold change >1.5 and FDR p<0.05) only at the one-day post-exposure group. The data obtained from the present study demonstrated that DEP/FSD inhalation exposure, under the conditions employed in the present study, resulted in only minimal changes in lung toxicity and gene expression profile in the rats.
2024-12-01 | GSE242155 | GEO
Project description:Human BEAS-2B bronchial epithelial cells were exposed directly at the air-liquid interphase towards exhaust gas and particles of a ship engine. The goal was to compare the responses towards different fuel combustions. The engine run either on diesel fuel (DF) or on Heavy Fuel Oil (HFO).
2015-02-01 | GSE63962 | GEO
Project description:We performed RNA sequencing to identify genes and pathways induced by Diesel exhaust particles exposure in WI-38 cells.
2021-02-14 | GSE166729 | GEO
Project description:Human BEAS-2B bronchial epithelial cells were exposed directly at the air-liquid interphase towards exhaust gas and particles of a ship engine. The goal was to compare the responses towards different fuel combustions. The engine run either on diesel fuel (DF) or on Heavy Fuel Oil (HFO). The lung cells were exposed 3 times to each combustion aerosol (DF or HFO). The duration of the exposure was 4h. The cells were seeded into transwell-inserts 24h before exposure. Within each exposure 3 transwell-inserts were exposed to the complete aerosol and 3 transwell-inserts were exposed to the filtered aerosol. Effects of the complete aerosol were referenced against the filtered aerosol to determine the effects of the aerosol particles.
2015-02-01 | E-GEOD-63962 | biostudies-arrayexpress
Project description:The potential of diesel exhaust particles (DEP) to transform human bronchial epithelial cells (HBEC3) was investigated and a stably transformed cell line (T2-HBEC3) was established. Short-term DEP exposure experiments adds information of immunomodulatory effect markers and differences in susceptibility between normal and sensitized bronhial epithelial cells of the human lung.
2017-11-30 | GSE107481 | GEO
Project description:Air pollution is an environmental risk factor linked to multiple human diseases including cardiovascular diseases (CVDs). While particulate matter (PM) emitted by diesel exhaust damages multiple organ systems, heart disease is one of the most severe pathologies affected by PM. However, the in vivo effects of diesel exhaust particles (DEP) on the heart and the molecular mechanisms of DEP-induced heart dysfunction have not been investigated. In the current study, we attempted to identify the proteomic signatures of heart fibrosis caused by diesel exhaust particles (DEP) in CVDs-prone apolipoprotein E knockout (ApoE-/-) mice model using tandem mass tag (TMT)-based quantitative proteomic analysis. DEP exposure induced mild heart fibrosis in ApoE-/- mice compared with severe heart fibrosis in ApoE-/- mice that were treated with CVDs-inducing peptide, angiotensin II. TMT-based quantitative proteomic analysis of heart tissues between PBS- and DEP-treated ApoE-/- mice revealed significant upregulation of proteins associated with platelet activation and TGFβ-dependent pathways. Our data suggest that DEP exposure could induce heart fibrosis, potentially via platelet-related pathways and TGFβ induction, causing cardiac fibrosis and dysfunction.
2023-12-09 | PXD045029 | Pride
Project description:Pulmonary effects of inhaled diesel particles in rats
| PRJNA640183 | ENA
Project description:Diesel exhaust particles (DEP), which contain hazardous compounds, are emitted during the combustion of diesel. As approximately one-third of the vehicles worldwide use diesel, there are growing concerns on the risks posed by DEP to human health. Long-term exposure to DEP is associated with airway hyperresponsiveness, pulmonary fibrosis, and inflammation; however, the molecular mechanisms behind the effects of DEP on the respiratory tract are poorly understood. Such mechanisms can be addressed by examining transcriptional and DNA methylation changes. In this study, we investigated the effect of 4 weeks exposure to 30 μg/ml DEP on DNA methylation levels in A549 cells.
2024-08-05 | GSE267215 | GEO
Project description:The pulmonary response to inhalation exposure to diesel exhaust particles (DEP) was investigated in a rat model. Adult male Sprague-Dawley rats were exposed by whole-body inhalation to air or an aerosol containing DEP at concentrations of 200 or 1000 mg/m3, 6 hours/day for 4 days. The control and DEP-exposed rats were euthanized at post-exposure time intervals of 1, 7, or 27 days and pulmonary inflammatory, cytotoxic and oxidant responses were determined. Analysis of bronchoalveolar lavage parameters of toxicity such as lactate dehydrogenase activity, oxidant generation, and inflammation did not reveal any significant pulmonary toxicity in the DEP-exposed rats. The lung gene expression profiles did not change significantly in the DEP exposed rats compared with the controls. The data obtained from the present study demonstrated that DEP inhalation exposure under the conditions employed in the present study did not result in any significant lung toxicity in the rats.
2022-12-31 | GSE152720 | GEO
Project description:Diesel exhaust particles (DEP), which contain hazardous compounds, are emitted during the combustion of diesel. As approximately one-third of the vehicles worldwide use diesel, there are growing concerns on the risks posed by DEP to human health. Long-term exposure to DEP is associated with airway hyperresponsiveness, pulmonary fibrosis, and inflammation; however, the molecular mechanisms behind the effects of DEP on the respiratory tract are poorly understood. Such mechanisms can be addressed by examining transcriptional and DNA methylation changes. In this study, we investigated the effect of 4 weeks exposure to 30 μg/ml DEP on gene expression levels in A549 cells.
2024-08-05 | GSE267213 | GEO