Project description:The increasing global human population has been associated with the development of high-density urban communities. This has led to increase in fossil energy consumption and posed serious threats to the environment and human health. Organosulfur compounds found in crude oil and transportation fuels such as diesel have gained strong attention because they are hazardous to human and the ecosystem. Moreover, the sulfur oxide gases resulting from fuel combustion are a major cause of acid rain. Governments and environmental organizations worldwide have recognized the problem and implemented strict regulations and legislations that limit the amount of sulfur in diesel. Hydrodesulphurization (HDS) is commonly used by oil refineries to reduce sulfur content in refined fuels. However, HDS has many disadvantages. It is costly, environmentally polluting, and not sufficiently efficient. Accordingly, there has been increasing interest in the development of alternative desulfurization technologies to circumvent the problems associated with the conventional HDS. Biodesulfurization (BDS) has emerged as an alternative or a complement technology to overcome the drawbacks of the conventional HDS. BDS exploits the ability of dedicated microorganisms to remove sulfur from many organosulfur compounds that are commonly found in crude oil and refined fuels. As compared to thermochemical treatments like HDS, BDS is environmentally friendly, cost-effective and active towards organosulfur compounds that escape the conventional HDS. Nonetheless, lack of deep understanding of the physiology and metabolism, particularly sulfur metabolism, of biodesulfurizing microbes has impeded the development and implementation of a commercially viable BDS process. In this project, we apply metabolomics and proteomics to better understand the physiological adaptations and sulfur metabolism of in a model biodesulfurization-competent strain Rhodococcus qingshengii IGTS8.
2021-08-09 | PXD021362 | Pride
Project description:Biodesulfurization of mixed organosulfur compounds
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.
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.
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 DEP dose sufficient to induce significant DNA methylation changes after four weeks of exposure.
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.
Project description:There is an emerging concern that particulate air pollution increases the risk of cranial nerve disease onset. Small nanoparticles, mainly derived from diesel exhaust particles reach the olfactory bulb by their nasal depositions. It has been reported that diesel exhaust inhalation causes inflammation of the olfactory bulb and other brain regions. However, these toxicological studies have not evaluated animal rearing environment. We hypothesized that rearing environment can change mice phenotypes and thus might alter toxicological study results. In this study, we exposed mice to diesel exhaust inhalation at 90 micro g/m3, 8 hours/day, for 28 consecutive days after rearing in a standard cage or environmental enrichment conditions. Microarray analysis found that expression levels of 112 genes were changed by diesel exhaust inhalation. Functional analysis using Gene Ontology revealed that the dysregulated genes were involved in inflammation and immune response. This result was supported by pathway analysis. Quantitative RT-PCR analysis confirmed 10 genes. Interestingly, background gene expression of the olfactory bulb of mice reared in a standard cage environment was changed by diesel exhaust inhalation, whereas there was no significant effect of diesel exhaust exposure on gene expression levels of mice reared with environmental enrichment. The results indicate for the first time that the effect of diesel exhaust exposure on gene expression of the olfactory bulb was influenced by rearing environment. Rearing environment, such as environmental enrichment, may be an important contributive factor to causation in evaluating still undefined toxic environmental substances such as diesel exhaust. RNA sample was taken from olfactory bulb of 56-day-old mouse received diesel exhaust (DE) inhalation at 90 micro g/m3, 8 hours/day, for 28 consecutive days, while control RNA was taken from mouse received clean air, after rearing in a standard cage or environmental enrichment conditions. Comparisons among groups were made by one-color method with normalized data from Cy3 channels for data analysis.
Project description:The marine bacterium Rhodococcus erythropolis PR4 was demonstrated to be able for assimilation/biodegradation of hydrocarbons. Not just the chromosome but two large plasmids provide versatile enzyme sets involved in many metabolic pathways. In order to identify the key elements involved in biodegradation of the model compound, hexadecane, and diesel oil, we performed whole transcriptome analysis on cells grown in the presence of n-hexadecane and diesel oil. Sodium acetate grown cells were used as control. The final goal of the project is a comparative transcriptomic analysis of Rhodococcus erythropolis PR4 cells grown on acetate, on the model compound: hexadecane and the real substrate: diesel oil. Comparative transcriptomics of Rhodococcus erythropolis PR4 grown on n-hexadecane, diesel oil, and sodium acetate.