Gene Expression Analysis of Carbonyl Sulfide Neurotoxicity
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE12018 | GEO | 2009/07/07
SECONDARY ACCESSION(S): PRJNA113293
REPOSITORIES: GEO
Similar Datasets
Project description:Gene Expression Analysis of Carbonyl Sulfide Neurotoxicity
| PRJNA113293 | ENA
Project description:Chlorpyrifos (CPF) is an organophosphorus pesticide (OP), and one of the most widely used pesticides in the world. Metabolites of CPF and other OPs continue to be identified in the majority of human samples, even in countries such as the United States where OP use is declining (Arcury et al., 2010). The effects of repeated occupational and environmental exposures to OPs are poorly understood, although human and animal studies consistently identify neurotoxicity as the primary endpoint of concern. Thus, occupational exposures to sublethal doses of CPF are consistently associated with problems in cognitive abilities, such as learning and memory but the biological mechanism(s) underlying this association remain speculative. To identify potential mechanisms of CPF neurotoxicity, we employed a rat model that simulated documented CPF exposures in Egyptian agricultural workers. We quantified mRNA expression profiles in the CA1 region of the hippocampus of adult male Long Evans (LE) rats administered CPF at 3 or 10 mg/kg/d (s.c.) for 21 days. Despite significant inhibition of cholinesterase activity by the end of the 21 d exposure period, the CPF-exposed rats displayed minimal signs of cholinergic toxicity. Distinct hippocampal mRNA and miRNA signatures were associated with CPF exposure. Toxicogenomics-based evidence identified increased expression of neuropeptide genes in the hippocampi of CPF-exposed rats, which have been shown to activate receptor-mediated signaling pathways involved in cell survival. The analysis of small non-coding RNA profiles suggested the possibility that miR132/212-mediated homeostatic regulatory pathways may also be activated by repeated exposures to CPF. These findings identify potential molecular effects that may contribute to neurobehavioral deficits.
2016-12-30 | GSE74676 | GEO
Project description:Chlorpyrifos (CPF) is an organophosphorus pesticide (OP), and one of the most widely used pesticides in the world. Metabolites of CPF and other OPs continue to be identified in the majority of human samples, even in countries such as the United States where OP use is declining (Arcury et al., 2010). The effects of repeated occupational and environmental exposures to OPs are poorly understood, although human and animal studies consistently identify neurotoxicity as the primary endpoint of concern. Thus, occupational exposures to sublethal doses of CPF are consistently associated with problems in cognitive abilities, such as learning and memory but the biological mechanism(s) underlying this association remain speculative. To identify potential mechanisms of CPF neurotoxicity, we employed a rat model that simulated documented CPF exposures in Egyptian agricultural workers. We quantified mRNA expression profiles in the CA1 region of the hippocampus of adult male Long Evans (LE) rats administered CPF at 3 or 10 mg/kg/d (s.c.) for 21 days. Despite significant inhibition of cholinesterase activity by the end of the 21 d exposure period, the CPF-exposed rats displayed minimal signs of cholinergic toxicity. Distinct hippocampal mRNA and miRNA signatures were associated with CPF exposure. Toxicogenomics-based evidence identified increased expression of neuropeptide genes in the hippocampi of CPF-exposed rats, which have been shown to activate receptor-mediated signaling pathways involved in cell survival. The analysis of small non-coding RNA profiles suggested the possibility that miR132/212-mediated homeostatic regulatory pathways may also be activated by repeated exposures to CPF. These findings identify potential molecular effects that may contribute to neurobehavioral deficits.
2016-12-30 | GSE74727 | GEO
Project description:Chlorpyrifos (CPF) is an organophosphorus pesticide (OP), and one of the most widely used pesticides in the world. Metabolites of CPF and other OPs continue to be identified in the majority of human samples, even in countries such as the United States where OP use is declining (Arcury et al., 2010). The effects of repeated occupational and environmental exposures to OPs are poorly understood, although human and animal studies consistently identify neurotoxicity as the primary endpoint of concern. Thus, occupational exposures to sublethal doses of CPF are consistently associated with problems in cognitive abilities, such as learning and memory but the biological mechanism(s) underlying this association remain speculative. To identify potential mechanisms of CPF neurotoxicity, we employed a rat model that simulated documented CPF exposures in Egyptian agricultural workers. We quantified mRNA expression profiles in the CA1 region of the hippocampus of adult male Long Evans (LE) rats administered CPF at 3 or 10 mg/kg/d (s.c.) for 21 days. Despite significant inhibition of cholinesterase activity by the end of the 21 d exposure period, the CPF-exposed rats displayed minimal signs of cholinergic toxicity. Distinct hippocampal mRNA and miRNA signatures were associated with CPF exposure. Toxicogenomics-based evidence identified increased expression of neuropeptide genes in the hippocampi of CPF-exposed rats, which have been shown to activate receptor-mediated signaling pathways involved in cell survival. The analysis of small non-coding RNA profiles suggested the possibility that miR132/212-mediated homeostatic regulatory pathways may also be activated by repeated exposures to CPF. These findings identify potential molecular effects that may contribute to neurobehavioral deficits.
2016-12-30 | GSE74726 | GEO
Project description:Male Sprague-dawley rats were exposed to saline, isopropyl alcohol, 1mg/kg, 3mg/kg or 6 mg/kg sulfur mustard for 30 min, 1 hr, 3 hr, 6 hr, or 24 hr before analysis of lung tissue by oligonucleotide array analysis. Keywords = sulfur mustard Keywords = rat Keywords = lung Keywords = bis-(2-chloroethyl) sulfide Keywords: ordered
2004-12-20 | GSE1888 | GEO
Project description:Treatment with chimeric antigen receptor (CAR) T-cell therapy targeting CD19 (CAR19) can cause neurotoxicity in patients. The role of microglia in CAR19-induced neurotoxicity was unclear. We observed morphological microglia alterations, increased production of GM-CSF, MCP-1 and TNF by microglia and neurocognitive deficits in B-cell lymphoma-bearing mice upon CAR19 transfer. Gene expression analysis was performed to determine the microglial activation and downstream signalling in response to CAR19 transfer.
2024-01-22 | GSE193696 | GEO
Project description:Stress response of Methylococcus capsulatus str.Bath toward hydrogen sulfide (H2S) was investigated via physiological study and transcriptomic profiling. M. capsulatus (Bath) can grow and tolerate up to 0.75%vol H2S in headspace. Vast change in pH suggests biological relevant sulfide oxidation. Dozens of H2S-sensitive genes were identified from comparison of cell transcriptome in different H2S concentrations. Mc sulfide quinone reductase (SQR) and persulfide dioxygenase were found to be active during sulfide detoxification. Moreover, xoxF, a novel lanthanide(Ln)-dependent methanol dehydrogenase (MDH) was overexpressed in H2S while mxaF, a calcium-dependent MDH, was down-regulated, and such MDH switch phenomenon is also well known to be induced by addition of lanthanide via an as-yet-unknown mechanism. Activities in quorum sensing and RND efflux pump also suggest their role in sulfide detoxification, and might provide insight on the xoxF/mxaF switch mechanism.
2021-12-24 | GSE192351 | GEO
Project description:The effect of sulfide stress on Desulfovibrio vulgaris Hildenborough (DvH) gene expression was determined by comparing the gene expression profiles of DvH under conditions in which sulfide was allowed to accumulate (high sulfide, average concentration 10 mM) against DvH cells grown under conditions in which sulfide was removed by continuous gassing (low sulfide, average concentration 1 mM). High sulfide significantly decreased the instantaneous growth rate constant and final cell density of the culture indicating a decreased bioenergetic fitness. Changes in gene expression caused by exposure to high sulfide were determined using full-genome DvH microarrays. The transcription of ribosomal protein-encoding genes was decreased, in agreement with the lower growth rate of DvH under high sulfide conditions. Interestingly, expression of the gene for DsrD, located downstream of the genes for dissimilatory sulfite reductase (DsrAB) was also strongly down-regulated. In contrast, the expression of many genes involved in iron accumulation, stress response and proteolysis, and chemotaxis were increased. This indicates that high sulfide represents a significant stress condition, in which the bioavailability of metals like iron may be lowered and in which proteins (e.g. metalloenzymes) may need to be refolded, or proteolytically degraded. Overall this leads to a reduced growth rate and less efficient biomass production with available resources.
2009-08-18 | GSE15073 | GEO
Project description:The effect of sulfide stress on Desulfovibrio vulgaris Hildenborough (DvH) gene expression was determined by comparing the gene expression profiles of DvH under conditions in which sulfide was allowed to accumulate (high sulfide, average concentration 10 mM) against DvH cells grown under conditions in which sulfide was removed by continuous gassing (low sulfide, average concentration 1 mM). High sulfide significantly decreased the instantaneous growth rate constant and final cell density of the culture indicating a decreased bioenergetic fitness. Changes in gene expression caused by exposure to high sulfide were determined using full-genome DvH microarrays. The transcription of ribosomal protein-encoding genes was decreased, in agreement with the lower growth rate of DvH under high sulfide conditions. Interestingly, expression of the gene for DsrD, located downstream of the genes for dissimilatory sulfite reductase (DsrAB) was also strongly down-regulated. In contrast, the expression of many genes involved in iron accumulation, stress response and proteolysis, and chemotaxis were increased. This indicates that high sulfide represents a significant stress condition, in which the bioavailability of metals like iron may be lowered and in which proteins (e.g. metalloenzymes) may need to be refolded, or proteolytically degraded. Overall this leads to a reduced growth rate and less efficient biomass production with available resources. For each condition 2 unique biological samples were hybridized to 4 arrays that each contained duplicate spots. Genomic DNA was used as universal reference.
2010-05-06 | E-GEOD-15073 | biostudies-arrayexpress