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Juvenile Fundulus heteroclitus exposed to Cr(VI)

ABSTRACT: Cr(VI) is a common bioavailable toxic metal that can cause oxidative stress, DNA adducts, and perturb normal gene expression. Changes in gene expression are useful biomarkers of toxicant exposure that provide information about the health of an organism, its ability to adapt to its environment, and indicate potential toxicant-specific effects. Therefore, we developed a toxicology array to the estuarine sentinel species Fundulus heteroclitus, or mummichog. Juvenile mummichog were exposed to potassium dichromate for thirty days at concentrations from 0 to 24 mg/L of Cr(VI), and growth was measured to determine the NOEC (1.5 mg/L or 0.0288 mM) and LOEC (3 mg/L or 0.0577 mM). Body burdens from Cr(VI) exposed fish demonstrated a dose dependent increase and were inversely correlated to body weight. Cr(VI)-exposed juvenile mummichog differentially expressed greater than 20 genes in a dose-dependent manner, including hepatic glucose transporter 2, liver fatty acid binding protein, ATPase synthase 8, type II keratin, TBT binding protein, and complement component C3-2. Many of these genes are involved in energy metabolism or growth, which is consistent with the reduced growth caused by Cr(VI). Keywords: dose response

ORGANISM(S): Pseudopleuronectes americanus Fundulus heteroclitus

PROVIDER: GSE3481 | GEO | 2006/03/31

SECONDARY ACCESSION(S): PRJNA93295

REPOSITORIES: GEO

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Adult male Fundulus heteroclitus exposed to Cr(VI)

Project description:Cr(VI) is a common bioavailable toxic metal that can cause oxidative stress, DNA adducts, and perturb normal gene expression. Changes in gene expression are useful biomarkers of toxicant exposure that provide information about the health of an organism, its ability to adapt to its environment, and indicate potential toxicant-specific effects. Therefore, we developed a toxicology array to the estuarine sentinel species Fundulus heteroclitus, or mummichog. Adults males were exposed to Cr(VI) for 7-days at 0, 1.5 (NOEC), or 3 mg/L (LOEC). Livers were excised and RNA isolated. Adults are used in the laboratory experiments so that we can compare laboratory studies to fish caught at chromium-contaminated field sites. Cr(VI) altered the expression of 12 genes in adult liver, including hepatic growth factor activator, heart fatty acid binding protein, and complement component C3-2. Keywords: dose response

2006-03-31 | GSE3480 | GEO

Long-term exposure to low-concentrations of Cr(VI) induce DNA damage and disrupt the transcriptional response to benzo[a]pyrene

Project description:Living organisms are exposed on a daily basis to widespread mixtures of toxic compounds. Mixtures pose a major problem in the assessment of health effects because they often generate substance-specific effects that cannot be attributed to a single mechanism. Two compounds often found together in the environment are the heavy metal chromium and the polycyclic aromatic hydrocarbon benzo[a]pyrene (B[a]P). We have examined how long-term exposure to a low concentration of Cr(VI) affects the transcriptional response to B[a]P, a second toxicant with an unrelated mechanism of action. Growth of mouse hepatoma cells for 20 passages in medium with 0.1 or 0.5 uM Cr(VI) increases DNA damage and apoptosis and decreases clonogenic ability. These cells also show transcriptome changes indicative of increased expression of DNA damage response and repair genes. In them, B[a]P activates cancer progression pathways, unlike cells never exposed to Cr(VI), where B[a]P activates mostly xenobiotic metabolism pathways. Cells grown in Cr(VI) for 20 passages and then cultured for an additional 5 passages in the absence of Cr(VI) recover from some but not all the chromium effects. They show B[a]P-dependent transcriptome changes strongly weighted towards xenobiotic metabolism, similar to those in B[a]P-treated cells that had no previous Cr(VI) exposure, but retain a high level of Cr(VI)-induced DNA damage and silence the expression of DNA damage and cancer progression genes. We conclude that the combined effect of these two toxicants appears to be neither synergistic nor cumulative, generating a toxic/adaptive condition that cannot be predicted from the effect of each toxicant alone. Mouse Hepa-1 cells treated with Cr, Bap, Cr+Bap and untreated were profiled using RNAseq in duplicates.

2013-08-07 | E-GEOD-49571 | biostudies-arrayexpress

Fundulus heteroclitus

Project description:Juvenile Fundulus heteroclitus exposed to Cr(VI)

| PRJNA93295 | ENA

Fundulus heteroclitus exposed to Cr(III)

Project description:Cr(III) is the dominant toxicant at some Superfund sites within the United States and therefore we are interested in its effects. Cr(III)’s mechanisms are not well studied or understood because of its low bioavailability. We have attempted to characterize the effects of Cr(III) on gene expression in the liver of adult male Fundulus heteroclitus. The NOEC and LOEC were determined at 32 and 64mg/L, respectively, by measuring growth after exposing juveniles for 30 days. Secondary exposures were performed with adult males at 32mg/L, livers excised, and RNA extracted. Microarrays were probed with cDNA from untreated or Cr(III)-exposed adult fish and gene expression was quantified. Cr(III) at 32mg/L altered the expression of 5 genes, including GSTalpha, GSTtheta, and ALDH4. Ultimately, we anticipate using this gene expression information to determine whether chromium is available at potentially adverse concentrations in contaminated sites. Keywords: dose response

2005-07-15 | GSE2807 | GEO

Long-term exposure to low-concentrations of Cr(VI) induce DNA damage and disrupt the transcriptional response to benzo[a]pyrene

2013-08-07 | GSE49571 | GEO

Environmental Pollutant Induced Epigenetic Predisposition to Developmental Defects and Cancer Phenotypes in the Progeny

Project description:Hexavalent Chromium, Cr(VI), exposure is known to cause cancer and is a significant human health concern. While the effect of Cr(VI) exposure on exposed individuals is well studied, long-term effects of the same on the progeny of exposed individual are not known. In this study, using Drosophila model system, we show that Cr(VI) exposure of mothers leads to phenotypic variations in the progeny who have never been exposed to Cr(VI). These phenotypic variations arise due to epigenetic instability in the somatic tissues of the progeny rather than novel genetic mutations. Using a Drosophila cancer model system, we also show that maternal Cr(VI) exposure can lead to cancer phenotypes in the progeny and the propensity to cause cancer phenotypes in the progeny is fixed in the population for at least three generations. Thus, we show for the first time that effects of Cr(VI) exposure can last for several generations. This study also lays the foundation to use Drosophila model system to provide novel insights into Cr(VI) and other heavy metal toxicity.

2019-01-01 | GSE111834 | GEO

Global transcriptional analysis of Cr(VI)-adapted cells of Klebsiella sp. AqSCr

Project description:Hexavalent chromium (Cr(VI)) is a highly toxic contaminant, some bacteria are able to transform it to less toxic and less soluble trivalent chromium (Cr(III)). Klebsiella sp. strain AqSCr, isolated from Cr(VI)-polluted groundwater, reduces Cr(VI) both aerobically and anaerobically, and resists up 35 mM of Cr(VI); Subculturing of AqSCr in the presence of Cr(VI) conduces to adaptation. In this study, we performed RNA-Seq of Cr(VI) adapted stage, finding 255 genes upregulated and 240 downregulated with respect to controls without Cr(VI). Genes differentially expressed are mostly associated with oxidative stress response, DNA repair and replication, sulfur starvation response, envelope-osmotic stress response, fatty acid metabolism, ribosomal subunits and energy metabolism. Among them, genes not previously associated with chromium resistance as cybB, encoding a putative superoxide oxidase, gltA2, encoding an alternative citrate synthase, and des, encoding a fatty acid desaturase were upregulated. The alternative sigma factors fecl, rpoE and rpoS were upredgulated in Cr(VI) adapted cells, then they participate in orchestate the Cr(VI)-resistance mechanisms in AqSCr strain

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Expression analysis in anaerobic Hanford 100H aquifer flow-through columns receiving lactate and chromate

Project description:Columns containing Hanford 100H aquifer sediment continuously infused with 5 mM lactate, 5 uM Cr(VI), and either 7.5 mM sulfate or 12 mM nitrate as an electron acceptor.

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Detect circulating miRNA Expression change after exposure to hexavalent chromium (an carcinogen) among occuaptional workers

Project description:We profiled plasma miRNA expression in workers exposed to Cr(VI), and assessed genetic damage on chromosome and DNA to compare the sensitivity between epigenetic changes and genetic damage for biomarkers We screened differently expressed plasma miRNAs between high and low Cr(VI) exposed workers using Agilent miRNA microarray. low exposure : <5.49 ng/ml; high exposure >5.49 ng/ml

2014-08-01 | E-GEOD-53135 | biostudies-arrayexpress

Crypt and villus transcriptomic responses in mouse small intestine following oral exposure to hexavalent chromium

Project description:Transcriptomic analyses were conducted separately on crypt and villus tissue from formalin-fixed paraffin-embedded transverse duodenal sections from the same study in which microarray-based analyses were previously conducted. A total of 28 groups (7 dose groups x 2 timepoints x 2 tissue compartments) were analyzed for differential gene expression, dose-response, and gene set enrichment. Tissue compartment isolation was confirmed by differences in expression of typical markers of crypt and villus compartments. Fewer than 21 genes were altered in the crypt compartment of mice exposed to 0.1-5 ppm Cr(VI) for 7 or 90 days, which increased to hundreds or thousands of genes at ≥20 ppm Cr(VI). Consistent with histological evidence for crypt proliferation, a significant, dose-dependent increase in genes that regulate mitotic cell cycle was prominent in the crypt, while subtle in the villus, when compared to samples from time-matched controls. Minimal transcriptomic evidence of DNA damage response in either the crypts or the villi is consistent with published in vivo genotoxicity data.

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