Gene expression profiling in Daphnia magna, Part III: Uncovering Biomarkers for Metal and ORC exposures
Ontology highlight
ABSTRACT:
ORGANISM(S): Daphnia magna
SUBMITTER: Xin Guan
PROVIDER: E-GEOD-13169 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Small organisms can be used as biomonitoring tools to assess chemicals in the environment. Chemical stressors are especially hard to assess and monitor when present as complex mixtures. Here, Daphnia magna were exposed for 24 hours to five different munitions constituents 2,4,6-trinitrotoluene (TNT), 2,4-dinitrotoluene (2,4-DNT), 2,6-dinitrotoluene (2,6-DNT), trinitrobenzene (TNB), dinitrobenzene (DNB), or 1,3,5-trinitro-1,3,5-triazacyclohexane (RDX) as well as to 8 different munitions mixtures and ground water contaminated with munitions constituents. To better understand possible mixture effects, gene expression changes from all treatments were compared using high-density microarrays. While mixtures and ground water exposures had genes and gene functions in common with single chemical exposures, unique functions were also affected, which was consistent with the non-additivity of chemical effects in these mixtures. The study consisted of three different experiments: (1) exposure to a concentration corresponding to 70% of 1/10th of the LC50 value of six individual MCs (TNT, 2,4-DNT, 2,6-DNT, DNB, TNB, RDX) and a control; (2) exposure to eight different laboratory mixtures of the previously mentioned MCs. Different combinations of MCs including four mixtures (Mixtures 5, 6, 7 and 8) representative of field collected groundwater from LAAP (Louisiana Army Ammunition Plant) were created; and (3) exposure to MC-contaminated ground water field-collected from 3 different wells (85, 108, and 141) at the LAAP. All exposures were conducted for 24h.
2011-06-22 | E-GEOD-30163 | biostudies-arrayexpress
Project description:Zinc Oxide nanoparticles (ZnO NPs) are being rapidly developed for use in consumer products, wastewater treatment and chemotherapy providing several possible routes for ZnO NP exposure to humans and aquatic organisms. Recent studies have shown that ZnO NPs undergo rapid dissolution to Zn+2, but the relative contribution of Zn+2 to ZnO NP bioavailability and toxicity is not clear. Gene expression profiling of D. magna exposed to ZnO NPs or ZnSO4 at equitoxic concentrations demonstrated that the particles cause toxicity through a distinct mechanism compared with Zn+2. D. magna were also exposed to a SiO NPs as a particle control at equimolar concentrations. The SiO NPs resulted in few differentially expressed genes and there was very little overlap between the genes affected by the ZnO NPs and the SiO NPs, suggesting that ZnO NPs cause a distinct pattern of differentially expressed genes. In the ZnO NP exposures, effects were observed to genes involved in cytoskeletal transport, cellular respiration and reproduction. Three biomarker genes including a multi-cystatin, ferritin and a C1q containing gene were confirmed as differentially expressed in a specific pattern by ZnO NP and provide a suite of biomarkers for identifying environmental exposure to ZnO NP and differentiating between NP and ionic exposure. We exposed Daphnia magna to the 1/10 LC50 and LC25 of ZnO nanoparticles and Zn++ as ZnSO4 for 24-h. For each exposure condition, we performed 3 exposures and 2 technical replicates (as dye swap) for each exposure (6 microarrays total). All exposures were compared to a unexposed laboratory control
2010-12-31 | E-GEOD-22051 | biostudies-arrayexpress
Project description:Munitions constituents (MCs) including hexahydro-1,3,5-trinitro-1,3,5-triazine (RDX), 2,4,6-trinitrotoluene (TNT), and TNT derivatives are recognized to elicit aberrant neuromuscular responses in many species. The onset of seizures resulting in death was observed in the avian model Northern bobwhite after oral dosing with RDX beginning at 8 mg/kg/day in subacute (14 days) exposures, whereas affective doses of the TNT derivative, 2,6-dinitrotoluene (2,6-DNT), caused gastrointestinal impacts, lethargy, and emaciation in subacute and subchronic (60 days) exposures. To assess and contrast the potential neurotoxicogenomic effects of these MCs, a Northern bobwhite microarray was developed consisting of 4119 complementary DNA (cDNA) features enriched for differentially-expressed brain transcripts from exposures to RDX and 2,6-DNT. RDX affected hundreds of genes in brain tissue, whereas 2,6-DNT affected few (M-bM-^IM-$ 17), indicating that 2,6-DNT exposure had relatively little impact on the brain in comparison to RDX. Birds exhibiting RDX-induced seizures accumulated over 20M-CM-^W more RDX in brain tissues in comparison to non-seizing birds even within a common dose. In parallel, expression patterns were unrelated among seizing and non-seizing birds exposed to equivalent RDX doses. In birds experiencing seizures, genes related to neuronal electrophysiology and signal transduction were significantly affected. Comparative toxicology revealed strong similarity in acute exposure effects between RDX and the organochlorine insecticide dichlorodiphenyltrichloroethane (DDT) regarding both molecular mechanisms and putative mode of action. In a manner similar to DDT, we hypothesize that RDX elicits seizures by inhibition of neuronal cell repolarization postaction potential leading to heightened neuronal excitability and seizures facilitated by multiple molecular mechanisms. Northern Bobwhite 60 Day 2,6-DNT Exposure, Brain Tissue Investigation (High Laser Intensity Scan): Juvenile male and female Northern bobwhite (12 weeks of age) were dosed with 2,6-DNT by daily gavage (0, 5, 10, 40, or 60 mg/kg/day). Each treatment group included 12 replicates per sex. Microarray experiments were conducted in a balanced interwoven-loop design using Cyanine-3 (Cy3) and A647. This experiment investigated the 60-day 2,6-DNT exposure comparing controls and the highest affective 2,6-DNT dose (60 mg/kg/day) in males and females, with all groups including three biological replicates for a total of 24 microarrays. To broaden signal detection, each microarray was scanned at high and low laser power to resolve low-intensity spots and reduce signal saturation, respectively (Skibbe et al., 2006). This dataset represents the High Intensity Scan.
2011-11-23 | E-GEOD-33919 | biostudies-arrayexpress
Project description:Munitions constituents (MCs) including hexahydro-1,3,5-trinitro-1,3,5-triazine (RDX), 2,4,6-trinitrotoluene (TNT), and TNT derivatives are recognized to elicit aberrant neuromuscular responses in many species. The onset of seizures resulting in death was observed in the avian model Northern bobwhite after oral dosing with RDX beginning at 8 mg/kg/day in subacute (14 days) exposures, whereas affective doses of the TNT derivative, 2,6-dinitrotoluene (2,6-DNT), caused gastrointestinal impacts, lethargy, and emaciation in subacute and subchronic (60 days) exposures. To assess and contrast the potential neurotoxicogenomic effects of these MCs, a Northern bobwhite microarray was developed consisting of 4119 complementary DNA (cDNA) features enriched for differentially-expressed brain transcripts from exposures to RDX and 2,6-DNT. RDX affected hundreds of genes in brain tissue, whereas 2,6-DNT affected few (M-bM-^IM-$ 17), indicating that 2,6-DNT exposure had relatively little impact on the brain in comparison to RDX. Birds exhibiting RDX-induced seizures accumulated over 20M-CM-^W more RDX in brain tissues in comparison to non-seizing birds even within a common dose. In parallel, expression patterns were unrelated among seizing and non-seizing birds exposed to equivalent RDX doses. In birds experiencing seizures, genes related to neuronal electrophysiology and signal transduction were significantly affected. Comparative toxicology revealed strong similarity in acute exposure effects between RDX and the organochlorine insecticide dichlorodiphenyltrichloroethane (DDT) regarding both molecular mechanisms and putative mode of action. In a manner similar to DDT, we hypothesize that RDX elicits seizures by inhibition of neuronal cell repolarization postaction potential leading to heightened neuronal excitability and seizures facilitated by multiple molecular mechanisms. Northern Bobwhite 60 Day 2,6-DNT Exposure, Brain Tissue Investigation (Low Laser Intensity Scan): Juvenile male and female Northern bobwhite (12 weeks of age) were dosed with 2,6-DNT by daily gavage (0, 5, 10, 40, or 60 mg/kg/day). Each treatment group included 12 replicates per sex. Microarray experiments were conducted in a balanced interwoven-loop design using Cyanine-3 (Cy3) and A647. This experiment investigated the 60-day 2,6-DNT exposure comparing controls and the highest affective 2,6-DNT dose (60 mg/kg/day) in males and females, with all groups including three biological replicates for a total of 24 microarrays. To broaden signal detection, each microarray was scanned at high and low laser power to resolve low-intensity spots and reduce signal saturation, respectively (Skibbe et al., 2006). This dataset represents the Low Intensity Scan.
2011-11-23 | E-GEOD-33928 | biostudies-arrayexpress
Project description:Munitions constituents (MCs) including hexahydro-1,3,5-trinitro-1,3,5-triazine (RDX), 2,4,6-trinitrotoluene (TNT), and TNT derivatives are recognized to elicit aberrant neuromuscular responses in many species. The onset of seizures resulting in death was observed in the avian model Northern bobwhite after oral dosing with RDX beginning at 8 mg/kg/day in subacute (14 days) exposures, whereas affective doses of the TNT derivative, 2,6-dinitrotoluene (2,6-DNT), caused gastrointestinal impacts, lethargy, and emaciation in subacute and subchronic (60 days) exposures. To assess and contrast the potential neurotoxicogenomic effects of these MCs, a Northern bobwhite microarray was developed consisting of 4119 complementary DNA (cDNA) features enriched for differentially-expressed brain transcripts from exposures to RDX and 2,6-DNT. RDX affected hundreds of genes in brain tissue, whereas 2,6-DNT affected few (M-bM-^IM-$ 17), indicating that 2,6-DNT exposure had relatively little impact on the brain in comparison to RDX. Birds exhibiting RDX-induced seizures accumulated over 20M-CM-^W more RDX in brain tissues in comparison to non-seizing birds even within a common dose. In parallel, expression patterns were unrelated among seizing and non-seizing birds exposed to equivalent RDX doses. In birds experiencing seizures, genes related to neuronal electrophysiology and signal transduction were significantly affected. Comparative toxicology revealed strong similarity in acute exposure effects between RDX and the organochlorine insecticide dichlorodiphenyltrichloroethane (DDT) regarding both molecular mechanisms and putative mode of action. In a manner similar to DDT, we hypothesize that RDX elicits seizures by inhibition of neuronal cell repolarization postaction potential leading to heightened neuronal excitability and seizures facilitated by multiple molecular mechanisms. Female Northern Bobwhite 14 Day 2,6-DNT Exposure, Brain Tissue Investigation (Low Laser Intensity Scan): Juvenile female Northern bobwhite (12 weeks of age) were dosed with 2,6-DNT by daily gavage (0, 50, 100, 190, or 350 mg/kg/day). Each treatment group included seven birds (at least three of each sex per treatment). Microarray experiments were conducted using an interwoven-loop design using Cyanine-3 (Cy3) and A647. This experiment investigated the effects of the 14-day 2,6-DNT exposure in females including controls, 60, and 100 mg/kg/day treatments, each including 3 biological replicates. To broaden signal detection, each microarray was scanned at high and low laser power to resolve low-intensity spots and reduce signal saturation, respectively (Skibbe et al., 2006). This dataset represents the Low Intensity Scan.
2011-11-22 | E-GEOD-33888 | biostudies-arrayexpress
Project description:Munitions constituents (MCs) including hexahydro-1,3,5-trinitro-1,3,5-triazine (RDX), 2,4,6-trinitrotoluene (TNT), and TNT derivatives are recognized to elicit aberrant neuromuscular responses in many species. The onset of seizures resulting in death was observed in the avian model Northern bobwhite after oral dosing with RDX beginning at 8 mg/kg/day in subacute (14 days) exposures, whereas affective doses of the TNT derivative, 2,6-dinitrotoluene (2,6-DNT), caused gastrointestinal impacts, lethargy, and emaciation in subacute and subchronic (60 days) exposures. To assess and contrast the potential neurotoxicogenomic effects of these MCs, a Northern bobwhite microarray was developed consisting of 4119 complementary DNA (cDNA) features enriched for differentially-expressed brain transcripts from exposures to RDX and 2,6-DNT. RDX affected hundreds of genes in brain tissue, whereas 2,6-DNT affected few (M-bM-^IM-$ 17), indicating that 2,6-DNT exposure had relatively little impact on the brain in comparison to RDX. Birds exhibiting RDX-induced seizures accumulated over 20M-CM-^W more RDX in brain tissues in comparison to non-seizing birds even within a common dose. In parallel, expression patterns were unrelated among seizing and non-seizing birds exposed to equivalent RDX doses. In birds experiencing seizures, genes related to neuronal electrophysiology and signal transduction were significantly affected. Comparative toxicology revealed strong similarity in acute exposure effects between RDX and the organochlorine insecticide dichlorodiphenyltrichloroethane (DDT) regarding both molecular mechanisms and putative mode of action. In a manner similar to DDT, we hypothesize that RDX elicits seizures by inhibition of neuronal cell repolarization postaction potential leading to heightened neuronal excitability and seizures facilitated by multiple molecular mechanisms. Female Northern Bobwhite 14 Day 2,6-DNT Exposure, Brain Tissue Investigation (High Laser Intensity Scan): Juvenile female Northern bobwhite (12 weeks of age) were dosed with 2,6-DNT by daily gavage (0, 50, 100, 190, or 350 mg/kg/day). Each treatment group included seven birds (at least three of each sex per treatment). Microarray experiments were conducted using an interwoven-loop design using Cyanine-3 (Cy3) and A647. This experiment investigated the effects of the 14-day 2,6-DNT exposure in females including controls, 60, and 100 mg/kg/day treatments, each including 3 biological replicates. To broaden signal detection, each microarray was scanned at high and low laser power to resolve low-intensity spots and reduce signal saturation, respectively (Skibbe et al., 2006). This dataset represents the High Intensity Scan.
2011-11-22 | E-GEOD-33893 | biostudies-arrayexpress
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2016-06-30 | E-GEOD-83859 | biostudies-arrayexpress
Project description:Applications for silver nanomaterials in consumer products are rapidly expanding, creating an urgent need for toxicological examination of the exposure potential and ecological effects of silver nanoparticles (AgNPs). The integration of genomic techniques into environmental toxicology has presented new avenues to develop exposure biomarkers and investigate the mode of toxicity of novel chemicals. In the present study we used a 15k oligonucleotide microarray for Daphnia magna, a freshwater crustacean and common indicator species for toxicity, to differentiate between particle specific and ionic silver toxicity and to develop exposure biomarkers for citrate-coated and PVP-coated AgNPs. Gene expression profiles revealed that AgNO3 and AgNPs have distinct expression profiles suggesting different modes of toxicity. However, the gene expression profiles of the different coated AgNPs were similar revealing similarities in the cellular effects of these two particles. Major biological processes disrupted by the AgNPs include protein metabolism and signal transduction. In contrast, AgNO3 caused a downregulation of developmental processes, particularly in sensory development. Metal responsive and DNA damage repair genes were induced by the PVP AgNPs, but not the other treatments. In addition, two specific biomarkers were developed for the environmental detection of PVP AgNPs; although further verification under different environmental conditions is needed. We exposed Daphnia magna to the 1/10 LC50 and LC25 of citrate coated and PVP-coated Ag nanoparticles and Ag+ as AgNO3 for 24-h. For each exposure condition, we performed 6 replicate exposures with 5 individuals in each. All exposures were compared to a unexposed laboratory control.
2012-08-04 | E-GEOD-35150 | biostudies-arrayexpress
Project description:Munitions constituents (MCs) including hexahydro-1,3,5-trinitro-1,3,5-triazine (RDX), 2,4,6-trinitrotoluene (TNT), and TNT derivatives are recognized to elicit aberrant neuromuscular responses in many species. The onset of seizures resulting in death was observed in the avian model Northern bobwhite after oral dosing with RDX beginning at 8 mg/kg/day in subacute (14 days) exposures, whereas affective doses of the TNT derivative, 2,6-dinitrotoluene (2,6-DNT), caused gastrointestinal impacts, lethargy, and emaciation in subacute and subchronic (60 days) exposures. To assess and contrast the potential neurotoxicogenomic effects of these MCs, a Northern bobwhite microarray was developed consisting of 4119 complementary DNA (cDNA) features enriched for differentially-expressed brain transcripts from exposures to RDX and 2,6-DNT. RDX affected hundreds of genes in brain tissue, whereas 2,6-DNT affected few (M-bM-^IM-$ 17), indicating that 2,6-DNT exposure had relatively little impact on the brain in comparison to RDX. Birds exhibiting RDX-induced seizures accumulated over 20M-CM-^W more RDX in brain tissues in comparison to non-seizing birds even within a common dose. In parallel, expression patterns were unrelated among seizing and non-seizing birds exposed to equivalent RDX doses. In birds experiencing seizures, genes related to neuronal electrophysiology and signal transduction were significantly affected. Comparative toxicology revealed strong similarity in acute exposure effects between RDX and the organochlorine insecticide dichlorodiphenyltrichloroethane (DDT) regarding both molecular mechanisms and putative mode of action. In a manner similar to DDT, we hypothesize that RDX elicits seizures by inhibition of neuronal cell repolarization postaction potential leading to heightened neuronal excitability and seizures facilitated by multiple molecular mechanisms. Male Northern Bobwhite 14 Day 2,6-DNT Exposure, Brain Tissue Investigation (Low Laser Intensity Scan): Juvenile male and female Northern bobwhite (12 weeks of age) were dosed with 2,6-DNT by daily gavage (0, 50, 100, 190, or 350 mg/kg/day). Each treatment group included seven birds (at least three of each sex per treatment). This microarray data set represents investigation of the male birds. Microarray experiments were conducted using an interwoven-loop design using Cyanine-3 (Cy3) and A647. This experiment investigated the effects of the 14-day 2,6-DNT exposure in males including controls and 60 mg/kg/day treatments, each including 3 biological replicates. To broaden signal detection, each microarray was scanned at high and low laser power to resolve low-intensity spots and reduce signal saturation, respectively (Skibbe et al., 2006). This dataset represents the Low Intensity Scan.
2011-11-23 | E-GEOD-33934 | biostudies-arrayexpress
Project description:Munitions constituents (MCs) including hexahydro-1,3,5-trinitro-1,3,5-triazine (RDX), 2,4,6-trinitrotoluene (TNT), and TNT derivatives are recognized to elicit aberrant neuromuscular responses in many species. The onset of seizures resulting in death was observed in the avian model Northern bobwhite after oral dosing with RDX beginning at 8 mg/kg/day in subacute (14 days) exposures, whereas affective doses of the TNT derivative, 2,6-dinitrotoluene (2,6-DNT), caused gastrointestinal impacts, lethargy, and emaciation in subacute and subchronic (60 days) exposures. To assess and contrast the potential neurotoxicogenomic effects of these MCs, a Northern bobwhite microarray was developed consisting of 4119 complementary DNA (cDNA) features enriched for differentially-expressed brain transcripts from exposures to RDX and 2,6-DNT. RDX affected hundreds of genes in brain tissue, whereas 2,6-DNT affected few (M-bM-^IM-$ 17), indicating that 2,6-DNT exposure had relatively little impact on the brain in comparison to RDX. Birds exhibiting RDX-induced seizures accumulated over 20M-CM-^W more RDX in brain tissues in comparison to non-seizing birds even within a common dose. In parallel, expression patterns were unrelated among seizing and non-seizing birds exposed to equivalent RDX doses. In birds experiencing seizures, genes related to neuronal electrophysiology and signal transduction were significantly affected. Comparative toxicology revealed strong similarity in acute exposure effects between RDX and the organochlorine insecticide dichlorodiphenyltrichloroethane (DDT) regarding both molecular mechanisms and putative mode of action. In a manner similar to DDT, we hypothesize that RDX elicits seizures by inhibition of neuronal cell repolarization postaction potential leading to heightened neuronal excitability and seizures facilitated by multiple molecular mechanisms. Male Northern Bobwhite 14 Day 2,6-DNT Exposure, Brain Tissue Investigation (High Laser Intensity Scan): Juvenile male and female Northern bobwhite (12 weeks of age) were dosed with 2,6-DNT by daily gavage (0, 50, 100, 190, or 350 mg/kg/day). Each treatment group included seven birds (at least three of each sex per treatment). This microarray data set represents investigation of the male birds. Microarray experiments were conducted using an interwoven-loop design using Cyanine-3 (Cy3) and A647. This experiment investigated the effects of the 14-day 2,6-DNT exposure in males including controls and 60 mg/kg/day treatments, each including 3 biological replicates. To broaden signal detection, each microarray was scanned at high and low laser power to resolve low-intensity spots and reduce signal saturation, respectively (Skibbe et al., 2006). This dataset represents the High Intensity Scan.
2011-11-23 | E-GEOD-33932 | biostudies-arrayexpress