Organismal sensitivity to environmental agents induced toxicity: A comparative ecotoxicogenomics approach
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ABSTRACT:
ORGANISM(S): Caenorhabditis elegans Drosophila melanogaster
PROVIDER: GSE98166 | GEO | 2018/12/01
REPOSITORIES: GEO
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Project description:To understand the role of genetic makeup in organismal tolerance/susceptibility we compared the Caenorhabditis elegans transcriptome profiles with those of Drosophila melanogaster. In this study, we exposed both organisms, to a synthetic chemical and evaluated their response at the transcriptome level, to gain insights to molecular players/pathways underlying organismal tolerance/susceptibility to xenobiotics
2018-12-01 | GSE98164 | GEO
Project description:To understand the role of genetic makeup in organismal tolerance/susceptibility we compared the Caenorhabditis elegans transcriptome profiles with those of Drosophila melanogaster. In this study, we exposed both organisms, to a synthetic chemical and evaluated their response at the transcriptome level, to gain insights to molecular players/pathways underlying organismal tolerance/susceptibility to xenobiotics
2018-12-01 | GSE98165 | GEO
Project description:Organismal sensitivity to environmental agents induced toxicity: A comparative ecotoxicogenomics approach
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Project description:Reactive oxygen species (ROS) such as hydrogen peroxide (H2O2) are well-described agents in physiology and pathology. Chronic inflammation causes incessant H2O2 generation associated with disease occurrences such as diabetes, autoimmunity, and cancer. In cancer, conditioning of the tumor microenvironment, e.g., hypoxia and ROS generation, has been associated with disease outcomes and therapeutic efficacy. Many reports have investigated the roles of the action of H2O2 across many cell lines and disease models. The genes predisposing tumor cell lines to H2O2-mediated demise are less deciphered, however. To this end, we performed in-house transcriptional profiling of 35 cell lines and simultaneously investigated each cell line's H2O2 inhibitory concentration (IC25) based on metabolic activity. More than 100-fold differences were observed between the most resistant and sensitive cell lines. Correlation and gene ontology pathway analysis identified a rigid association with genes intertwined in cell cycle progression and proliferation, as such functional categories dominated the top ten significant processes. The ten most substantially correlating genes (Spearman r > 0.70 or < -0.70) were validated using qPCR, showing complete congruency with microarray analysis findings. Western blotting confirmed the correlation of cell cycle-related proteins negatively correlating with H2O2 IC25. Top genes related to ROS production or antioxidant defense were only modest in correlation (Spearman r > 0.40 or < -0.40). In conclusion, our in-house transcriptomic correlation analysis revealed a set of cell cycle-associated genes associated with a priori resistance or sensitivity to H2O2-induced cellular demise with the detailed and causative roles of individual genes remaining unclear.
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Project description:In Her2-positive breast cancer patients, inhibition of epidermal growth factor receptor 2 (ErbB2)-signaling is often combined with chemotherapy and radiotherapy. The risk of cardiac toxicity after anthracyclines and radiotherapy is recognized, but little is known about increased risk when these treatments are combined with ErbB2 inhibition. This study investigated whether ErbB2 inhibition increased radiation or anthracycline-induced toxicity. In an in vitro study, human cardiomyocytes were treated with irradiation or doxorubicin, alone or in combination with trastuzumab, and evaluated for cell survival and growth. Groups of mice received 0 or 14 Gy to the heart, alone or in combination with lapatinib, or 3 × 4 mg/kg doxorubicin alone or in combination with lapatinib. Mice were evaluated 40 weeks after treatment for cardiac damage. Changes in cardiac function ((99m)Tc-Myoview gated SPECT) were related to histomorphology and microvascular damage. Radiation or doxorubicin-induced cardiomyocyte toxicity (in vitro) were not exacerbated by trastuzumab. Cardiac irradiation of mice decreased microvascular density (MVD) and increased endothelial damage in surviving capillaries (decrease alkaline phosphatase expression and increased von Willebrand factor), but these changes were not exacerbated by lapatinib. Inflammatory responses in the irradiated epicardium (CD45+ and F4/80+ cells) were significantly reduced in combination with lapatinib. Irradiation, doxorubicin, and lapatinib each induced cardiac fibrosis but this was not further enhanced when treatments were combined. At the ultra-structural level, both lapatinib and doxorubicin induced mitochondrial damage, which was enhanced in combined treatments. Lapatinib alone also induced mild changes in cardiac function but this was not enhanced in the combined treatments. Trastuzumab did not enhance direct radiation or anthracycline toxicity of cardiomyocytes in vitro. Lapatinib did not enhance the risk of radiation or anthracycline-induced cardiac toxicity in mice up to 40 weeks after treatment, but mitochondrial damage was more severe after doxorubicin combined with lapatinib.
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Project description:AimsThe purpose of this study was to evaluate the effects of altered environmental conditions on the persistence of Francisella tularensis bacteria and Venezuelan equine encephalitis virus (VEEV), on two material types.Methods and resultsFrancisella tularensis (F.t.) and VEEV were inoculated (c. 1 × 108 colony-forming units or PFU), dried onto porous and nonporous fomites (glass and paper), and exposed to combinations of altered environmental conditions ranging from 22 to 60°C and 30 to 75% relative humidity (RH). Viability of test organism was assessed after contact times ranging from 30 min to 10 days. Inactivation rates of F.t. and VEEV increased as both temperature and/or RH were increased. Greater efficacy was observed for paper as compared to glass for both test organisms.ConclusionsThe use of elevated temperature and RH increased rate of inactivation for both organisms and greater than six log reduction was accomplished in as little as 6 h by elevating temperature to approximately 60°C.Significance and impact of the studyThese results provide information for inactivation of nonspore-forming select agents using elevated temperature and humidity which may aid incident commanders following a biological contamination incident by providing alternative methods for remediation.
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