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Project description:Bioassay is a system for monitoring toxicity of chemicals in the environment via the biological responses of experimental organisms. These responses can be detected by analysis of genome-wide changes in mRNA expression levels using DNA microarray. We applied this system for evaluation of synergistic toxicity by cadmium and thiuram, as this combination showed mutual growth inhibition in yeast. Hierarchical cluster analysis using the mRNA expression profiles suggested the response of yeast to this combination is similar to that seen with cadmium treatment. Functional characterization of induced genes by this combination treatment also suggests the enhanced toxicity of cadmium. This toxicity was observed as the damage to mitochondrial functions which were not observed with either cadmium or thiuram treatments alone. The potential toxicity to mitochondria by this combinational treatment was confirmed as the result of mitochondrial curing. We could evaluate the synergistic toxicity by cadmium and thiuram and show the possible use of transcriptome bioassay for synergistic toxicity. Keywords: stress response
2007-09-01 | GSE8718 | GEO
Project description:The “Fish Acute Toxicity Test” in the “OECD Guideline for Testing of Chemicals” is an essential test for environmental toxicity. Here we have tried to evaluate the physiology of medaka during this test procedure by using genomics. Genomics technology can provide genome-wide expression profiles of mRNA, and these profiles correspond to the physiology of organisms. Thus, a comparison of mRNA expression profiles gives information on the reproducibility of experimental conditions. Expression profiles of mRNA were measured for medakas maintained within the allowable range of the test conditions and also under extreme conditions beyond the guidelines limits. We confirmed the high physiological reproducibility of medaka kept in the recommended conditions of the “Fish Acute Toxicity Test” in the “OECD Guideline for Testing of Chemicals" from the expression profiles obtained under all experimental conditions except for the type of feeding.
2010-07-22 | GSE15380 | GEO
Project description:Thorium (232Th), an actinoide element, is among the most common and naturally occurring radioactive materials distributed in our environment. Thorium has been used as a radiographic contrast agent (thorotrast) from 1930 to 1955, and many studies on its effects to the human body have been reported. Once thorium is injected in the body, the risk of cancer is increased by the direct bombardment from alpha-particle with high linear energy transfer during decay of Thorium. However, these many reports focus on the irradiation damage by long-term exposure of thorium. The acute toxicity of thorium is greater risk from the chemical toxicity than from the radiological toxicity. Here, we evaluated the effect of thorium from the stand point of chemical toxicity using yeast DNA microarray. In this experiment, genes that contribute to “C-compound and carbohydrate metabolism”, “energy”, and “cell rescue, defense and virulence” were significantly induced. These genes were classified into oxidative stress, glycogen and trehalose metabolism, sugar transport, and cell wall damage. On the contrary, only one gene related to DNA damage was detected. These results indicate that thorium causes the damage of cell wall and induces the oxidative stress. In order to overcome oxidative stress, yeast cells promote the glycogen and trehalose metabolisms and shift to anaerobic fermentation. Keywords: stress response
2007-11-01 | GSE9463 | GEO
Project description:Although nickel exposure results in allergic reactions, respiratory conditions, and cancer in humans and rodents, the ramifications of excess nickel in the environment for animal and human health remain largely undescribed. Nickel and other cationic metals travel through waterways and bind to soils and sediments. To evaluate the potential toxic effects of nickel at environmental contaminant levels (8.9-7,600 µg Ni/g dry weight of sediment and 50-800 µg NiCl2/L of water), we conducted assays using two cosmopolitan nematodes, Caenorhabditis elegans and Pristionchus pacificus. We assayed the effects of both sediment-bound and aqueous nickel upon animal growth, developmental survival, lifespan, and fecundity. Uncontaminated sediments were collected from sites in the Midwestern United States and spiked with a range of nickel concentrations. We found that nickel-spiked sediment substantially impairs both survival from larval to adult stages and adult longevity in a concentration-dependent manner. Further, while aqueous nickel showed no adverse effects on either survivorship or longevity, we observed a significant decrease in fecundity, indicating that aqueous nickel could have a negative impact on nematode physiology. Intriguingly, C. elegans and P. pacificus exhibit similar, but not identical, responses to nickel exposure. Moreover, P. pacificus could be tested successfully in sediments inhospitable to C. elegans. Our results add to a growing body of literature documenting the impact of nickel on animal physiology, and suggest that environmental toxicological studies could gain an advantage by widening their repertoire of nematode species.
| S-EPMC3792034 | biostudies-literature
Project description:The effect, if any, of age on the pulmonary toxicity induced by Min-U-Sil 5 crystalline silica exposure was investigated in rats. As part of the study, the changes in global gene expression profiles in the blood and lungs of the animals were determined. To conduct these studies, to determine if age influences the pulmonary response to crystalline silica exposure, two different age groups of healthy, male F344 rats were used. In this study the young age group of rats (6 months old at the time of exposure) was exposed to either air or crystalline silica (Min-U-Sil 5) (15 mg/m3, 6 hours/day, 5 days) by whole body inhalation. The young age group of rats simulates a group of workers who would be 18 to 20 years old. At two crystalline silica post-exposure time periods (1-day and 6-months) animals were euthanized and pulmonary inflammatory, cytotoxic, and oxidant responses were determined. Analysis of bronchoalveolar lavage parameters of toxicity such as oxidant generation and inflammation revealed significant changes in pulmonary toxicity in the crystalline silica exposed rats compared with the time-matched, air exposed control rats. The blood gene expression profiles showed only minimal changes, at both the time points, in the crystalline silica exposed rats compared with the controls. Specifically, there were a total of 5 genes significantly differentially expressed (fold change >1.5 and FDR p<0.05) in the one-day post-exposure group and no significantly differentially genes in the 6-month post-exposure group. However, the lung gene expression profiles showed substantial changes in the crystalline silica exposed animals at both one-day and 6-month post-exposure. Specifically, there were a total of 385 genes significantly differentially expressed (fold change >1.5 and FDR p<0.05) at the one-day post-exposure group and 317 genes significantly differentially expressed at the 6-month post-exposure. The data obtained from the present study demonstrated that crystalline silica inhalation exposure, under the conditions employed in the present study, resulted in significant changes in lung toxicity parameters and lung gene expression profile in the rats at both 1-day and 6-month post-exposure.
2024-12-01 | GSE247344 | GEO
Project description:Amyloid beta 42 (Abeta42) is the principal trigger of neurodegeneration during Alzheimer’s disease (AD); however, the etiology of Abeta42 toxicity remains elusive. In a proteomic approach using a yeast model for intracellular Abeta42 toxicity, we here identify the HSP40 family member Ydj1, the yeast orthologue of human DnaJA1, as a crucial factor in Abeta42-mediated toxicity.
2022-04-27 | PXD012612 | Pride
Project description:Disruption of protein quality control can be detrimental, having toxic effects on single cell organisms, and causing neurodegenerative diseases such as Alzheimer’s, Parkinson’s and Huntington’s in humans. Here we examined the effects of polyQ aggregation in a major fungal pathogen of humans, Candida albicans, with the goal of identifying new approaches to disable this fungus. However, we discovered that expression of poly-glutamine (polyQ) stretches up to 230Q had no effect on C. albicans ability to grow and withstand proteotoxic stress. Bioinformatics analysis demonstrates that C. albicans has a similarly glutamine rich proteome to the unicellular fungus Saccharomyces cerevisiae, which exhibits polyQ toxicity with as few as 72Q. Surprisingly, global transcriptional profiles indicated no significant change upon induction of up to 230Q. Proteomic analysis highlighted two key interactors of 230Q, Sis1 and Sgt2, however, loss of either protein had no additional effect on C. albicans toxicity. Our data suggest that C. albicans has evolved powerful mechanisms to overcome aggregation prone proteins, providing a unique model for studying polyQ associated diseases.
2016-12-05 | PXD003916 | Pride
Project description:The effect, if any, of age on the pulmonary toxicity induced by Min-U-Sil 5 crystalline silica exposure was investigated in rats. As part of the study, the changes in global gene expression profiles in the blood and lungs of the animals were determined. To conduct these studies, to determine if age influences the pulmonary response to crystalline silica exposure, two different age groups of healthy, male F344 rats were used. In this study the old age group of rats (12 months old at the time of exposure) was exposed to either air or crystalline silica (Min-U-Sil 5) (15 mg/m3, 6 hours/day, 5 days) by whole body inhalation. The old age group of rats simulates a group of workers who would be 45 to 50 years old. At two crystalline silica post-exposure time periods (1-day and 6-months) animals were euthanized and pulmonary inflammatory, cytotoxic, and oxidant responses were determined. Analysis of bronchoalveolar lavage parameters of toxicity such as oxidant generation and inflammation revealed significant changes in pulmonary toxicity in the crystalline silica exposed rats compared with the time-matched, air exposed control rats. The blood gene expression profiles showed only minimal changes, at both the time points, in the crystalline silica exposed rats compared with the controls. Specifically, no genes were significantly differentially expressed (fold change >1.5 and FDR p<0.05) in the one-day post-exposure group and only 6 genes were significantly differentially expressed in the 6-month post-exposure group. However, the lung gene expression profiles showed substantial changes in the crystalline silica exposed animals at both one-day and 6-month post-exposure. Specifically, there were a total of 325 genes significantly differentially expressed (fold change >1.5 and FDR p<0.05) at the one-day post-exposure group and 3348 genes significantly differentially expressed at the 6-month post-exposure. The data obtained from the present study demonstrated that crystalline silica inhalation exposure, under the conditions employed in the present study, resulted in significant changes in lung toxicity parameters and lung gene expression profile in the rats at both 1-day and 6-month post-exposure.
2024-12-01 | GSE250537 | GEO