Chemical exposures in fish have been linked to loss of olfaction leading to an inability to detect predators and prey and decreased survival. However, the mechanisms underlying olfactory neurotoxicity are not well characterized, especially in environmental exposures which involve chemical mixtures. We used zebrafish to characterize olfactory transcriptional responses by two model olfactory inhibitors, the pesticide chlorpyrifos (CPF) and mixtures of CPF with the neurotoxic metal copper (Cu).
Transcriptional biomarkers and mechanisms of copper-induced olfactory injury in zebrafish.
Specimen part, Treatment
View SamplesThe purpose of this study was to identify transcripts differentially expressed in zebrafish embryos exposed to two oxygenated PAHs, 1,9-benz-10-anthrone and benzanthracene-7,12-dione, which cause abnormal development. Overall design: We used RNA-seq (Illumina HiSeq) to identify mRNA profiles of whole zebrafish embryos exposed to 10 µM 1,9-benz-10-anthrone, benzanthracene-7,12-dione or vehicle control (1% DMSO) from 6-48 hours post fertilization
Ligand-Specific Transcriptional Mechanisms Underlie Aryl Hydrocarbon Receptor-Mediated Developmental Toxicity of Oxygenated PAHs.
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View SamplesDomoic acid (DA) is a neuroexcitatory amino acid that is naturally produced by some marine diatom species of the genus Pseudo-nitzschia. Ingestion of DA-contaminated seafood by humans results in a severe neurotoxic disease known as amnesic shellfish poisoning (ASP). Clinical signs of ASP include seizures and neuronal damage from activation of AMPA and kainate receptors. However, the impacts of DA exposure at levels below those known to induce outward signs of neurobehavioral exicitotoxicity have not been well characterized. To further understand the mechanisms of neurotoxic injury associated with DA exposure, we examined the transcriptome of whole brains from zebrafish (Danio rerio) receiving intracoelomic (IC) DA at both symptomatic and asymptomatic doses. A majority of zebrafish exposed to high-dose DA (1.2 g DA/g) exhibited clinical signs of neuroexcitotoxicity (EC50 of 0.86 g DA/g) within 5 to 20 minutes of IC injection. All zebrafish receiving low-dose DA (0.47 g DA/g) or vehicle only maintained normal behavior. Microarray analysis of symptomatic and asymptomatic exposures collectively yielded 306 differentially expressed genes (1.5-fold, p = 0.05) predominately represented by signal transduction, ion transport, and transcription factor functional categories. Transcriptional profiles were suggestive of neuronal apoptosis following an overwhelming of protective adaptive pathways. Further, potential molecular biomarkers of neuropathic injury, including Nrdg4, were identified and may be relevant to DA exposure levels below that causing neurobehavioral injury. Our results validate zebrafish as a vertebrate model to study mechanisms of DA neurotoxicity and provide a basis for identifying pathways of DA-induced injury as well as biomarkers of asymptomatic and symptomatic DA exposure levels.
Gene expression profiles in zebrafish brain after acute exposure to domoic acid at symptomatic and asymptomatic doses.
No sample metadata fields
View SamplesTo identify biosignatures that describe these lifestyle susceptibility factors, we performed parallel exposures of regular weight (RW) C57BL/6 and diet-induced obese (DIO) C57BL/6 mice to cigarette smoke, either mainstream (MS) or sidestream (SS), mimicking both the smoker and environmental exposure through second-hand smoke, respectively.
Impaired transcriptional response of the murine heart to cigarette smoke in the setting of high fat diet and obesity.
Specimen part, Treatment
View SamplesTo identify biosignatures that describe these lifestyle susceptibility factors, we performed parallel exposures of regular weight (RW) C57BL/6 and diet-induced obese (DIO) C57BL/6 mice to cigarette smoke, either mainstream (MS) or sidestream (SS), mimicking both the smoker and environmental exposure through second-hand smoke, respectively.
Impaired transcriptional response of the murine heart to cigarette smoke in the setting of high fat diet and obesity.
Specimen part, Treatment
View SamplesTo identify key biological pathways that define susceptibility factors for pulmonary infection during obesity, diet-induced obese (DIO) and regular weight (RW) C57BL/6 mice were exposed to 0.5 g/L inhaled lipopolysaccharide (LPS) for 1 hr/d for 4 days over a period of 2 weeks.
Diet-induced obesity reprograms the inflammatory response of the murine lung to inhaled endotoxin.
Specimen part
View SamplesTo investigate how the phenotype of macrophages that have engulfed engineered nanoparticles (ENPs) differs from normal macrophages, we conducted Affymetrix microarray studies to identify the gene regulatory pathways affected by the ENPs. To mimic potential occupational exposure scenarios, the experimental design involved pretreatment of mouse primary bone marrow macrophages with the ENPs (25 mg/ml) for 24 hr, followed by removal of residual ENPs and challenging the macrophages with the TLR4 ligand and surrogate bacterial stimulus, lipopolysachharide (LPS) for 4 hr. The 4 hr challenge time was chosen based on preliminary studies which showed many of the proinflammatory gene expression responses peak between 2-6 hr after LPS treatment.
Dysregulation of macrophage activation profiles by engineered nanoparticles.
Specimen part, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Three human cell types respond to multi-walled carbon nanotubes and titanium dioxide nanobelts with cell-specific transcriptomic and proteomic expression patterns.
Specimen part, Cell line, Treatment, Time
View SamplesTo identify key biological pathways that define toxicity or biocompatibility after nanoparticle exposure, three human cell types were exposed in vitro to two high aspect ratio nanoparticles for 1 hr or 24 hr and collected for global transcriptomics.
Three human cell types respond to multi-walled carbon nanotubes and titanium dioxide nanobelts with cell-specific transcriptomic and proteomic expression patterns.
Specimen part, Cell line, Treatment, Time
View SamplesTo identify key biological pathways that define toxicity or biocompatibility after nanoparticle exposure, three human cell types were exposed in vitro to two high aspect ratio nanoparticles for 1 hr or 24 hr and collected for global transcriptomics.
Three human cell types respond to multi-walled carbon nanotubes and titanium dioxide nanobelts with cell-specific transcriptomic and proteomic expression patterns.
Specimen part, Cell line, Treatment, Time
View Samples