The role of microbial mats in the removal of hexavalent chromium and associated shifts in their bacterial community composition
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PROVIDER: PRJEB33895 | ENA |
REPOSITORIES: ENA
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Project description:Significant occupational and environmental exposures to hexavalent chromium, a metal with broad toxicity potential in humans, have been reported. In order to understand the mechanisms of dermal toxicity induced by hexavalent chromium, global gene expression profiling of human dermal fibroblasts exposed to a toxic concentration of potassium dichromate was performed. Microarray analysis of the gene expression profile in the fibroblasts treated with potassium dichromate identified significant differential expression of approximately 1,200 transcripts compared with the control cells. Hierarchical cluster analysis of the gene expression profile demonstrated a clear separation of the treated cells from the control group of cells. Functional categorization of the differentially expressed genes identified the enrichment of genes involved in several cellular processes, including apoptosis and oxidative stress, in the fibroblasts exposed to hexavalent chromium. Induction of apoptosis and generation of hydroxyl radicals indicative of oxidative stress in the dermal fibroblasts in response to their exposure to hexavalent chromium were independently confirmed by TUNEL assay and electron spin resonance (ESR) analysis, respectively. The potassium dichromate-induced cytotoxicity, differential gene expression, apoptosis, and oxidative stress were significantly blocked by the addition of ferrous sulfate, an agent known for its ability to reduce hexavalent chromium to the insoluble and therefore impermeable trivalent form, to the cell culture medium. Taken together, our data provide insights into the potential mechanisms underlying the dermal toxicity of hexavalent chromium and suggest a definite role for apoptosis and oxidative stress in Cr(VI)-induced cytotoxicity in human dermal fibroblasts.
2011-07-31 | GSE16349 | GEO
Project description:Significant occupational and environmental exposures to hexavalent chromium, a metal with broad toxicity potential in humans, have been reported. In order to understand the mechanisms of dermal toxicity induced by hexavalent chromium, global gene expression profiling of human dermal fibroblasts exposed to a toxic concentration of potassium dichromate was performed. Microarray analysis of the gene expression profile in the fibroblasts treated with potassium dichromate identified significant differential expression of approximately 1,200 transcripts compared with the control cells. Hierarchical cluster analysis of the gene expression profile demonstrated a clear separation of the treated cells from the control group of cells. Functional categorization of the differentially expressed genes identified the enrichment of genes involved in several cellular processes, including apoptosis and oxidative stress, in the fibroblasts exposed to hexavalent chromium. Induction of apoptosis and generation of hydroxyl radicals indicative of oxidative stress in the dermal fibroblasts in response to their exposure to hexavalent chromium were independently confirmed by TUNEL assay and electron spin resonance (ESR) analysis, respectively. The potassium dichromate-induced cytotoxicity, differential gene expression, apoptosis, and oxidative stress were significantly blocked by the addition of ferrous sulfate, an agent known for its ability to reduce hexavalent chromium to the insoluble and therefore impermeable trivalent form, to the cell culture medium. Taken together, our data provide insights into the potential mechanisms underlying the dermal toxicity of hexavalent chromium and suggest a definite role for apoptosis and oxidative stress in Cr(VI)-induced cytotoxicity in human dermal fibroblasts. 16 samples were analyzed in this experiment. Exponentially growing human dermal fibroblasts (3x105 cells) were cultured in T25 cell culture flasks. When the cells were approximately 70% confluent, hexavalent potassium dichromate (5µM) was added to the medium with or without 40µM ferrous sulfate. Following 16 hours of culturing at 37oC, total RNA was isolated for gene expression studies. Details of the samples are: Control 4 Samples: Cr(0)-1, Cr(0)-2, Cr(0)-3, Cr(0)-4 Cr 5 µM 4 Samples: Cr(5)-5, Cr(5)-6, Cr(5)-7, Cr(5)-8 FeSO4 40 µM 4 Samples: Fe(40)-9, Fe(40)-10, Fe(40)-11, Fe(40)-12 Cr 5 µM + FeSO4 40 µM 4 Samples: Cr(5)+Fe(40)-13,Cr(5)+Fe(40)-14, Cr(5)+Fe(40)-15, Cr(5)+Fe(40)-16
2011-07-30 | E-GEOD-16349 | biostudies-arrayexpress
Project description:In vivo transcription profiling in Drosophila melanogaster larvae exposed to hexavalent chromium
2023-05-03 | E-MEXP-3245 | biostudies-arrayexpress
Project description:In order to evaluate the mechanisms underlying hexavalent chromium (Cr(VI)) responses, mice and rats were treated with varying concentrations of Cr(VI) in drinking water, as sodium dichromate dihydrate (SDD). Potential transcriptomic responses were evaluated through microarray analysis.
2016-09-24 | GSE87261 | GEO
Project description:In order to evaluate the mechanisms underlying hexavalent chromium (Cr(VI)) responses, mice and rats were treated with varying concentrations of Cr(VI) in drinking water, as sodium dichromate dihydrate (SDD). Potential transcriptomic responses were evaluated through microarray analysis.
2016-09-24 | GSE87259 | GEO
Project description:Microbial mats are rarely reported for chromium-polluted ecosystems, hence information on their bacterial diversity and role in chromium removal are very scarce. We investigated the role of nine microbial mats, collected from three quarry sumps of chromium mining sites, in the removal of hexavalent chromium [Cr(VI)]. Bacterial diversity in these mats and community shifts after incubation with Cr(VI) have been investigated using MiSeq sequencing. In nature, a chromium content of 1,911 ± 100 mg kg-1 was measured in the microbial mats, constituting the third highest source of environmentally available chromium. The mats were able to remove 1 mg l-1 of Cr(VI) in 7 days under aerobic conditions. MiSeq sequencing of the original mats yielded 46-99% of the sequences affiliated to Proteobacteria, Firmicutes and Actinobacteria. When the mats were incubated with Cr(VI), the bacterial community shifted in the favor of Alphaproteobacteria and Verrucomicrobiae. We conclude that microbial mats in the quarry sumps harbor diverse microorganisms with the ability to remove toxic Cr(VI), hence these mats can be potentially used to remove chromium from polluted waters.
| S-EPMC7001535 | biostudies-literature
Project description:Hexavalent chromium compounds are well-established respiratory carcinogens utilized in industrial processes. While inhalation exposure constitutes an occupational risk affecting mostly chromium workers, environmental exposure from drinking water is a widespread gastrointestinal carcinogen, affecting millions of people throughout the world. Cr(VI) is genotoxic, by forming protein-Cr-DNA adducts and silencing tumor suppressor genes, but its mechanism of action at the molecular level is poorly understood. We have used FAIRE to show that Cr(VI) elicits broad changes in chromatin accessibility resulting from disruption of the binding of transcription factors CTCF and AP-1 to their cognate sites in chromatin. Here, we have used two complementary approaches to test the hypothesis that chromium perturbs chromatin organization and dynamics. DANPOS2 analyses of MNase.seq data identified several chromatin alterations induced by Cr(VI) affecting nucleosome architecture, including occupancy changes at specific genome locations; position shifts of 10 nucleotides or more; and fuzziness, or changes in signal amplitude. Using ATAC to analyze changes in chromatin accessibility, we found that Cr(VI) opened differentially accessible chromatin domains in a dose-dependent manner. These domains were enriched for the previously identified binding motifs for CTCF and AP-1, many located in promoters of differentially expressed genes. Cr(VI)-enriched CTCF sites were confirmed by ChIP.seq and, when compared with ENCODE-validated CTCF site datasets from mouse liver, correlated with evolutionarily conserved similar sites occupied in vivo. Our results show that Cr(VI) exposure promotes broad changes in chromatin accessibility and suggest that the subsequent dysregulation of transcription may result from the disruption of CTCF binding and nucleosome spacing, suggesting that transcription regulatory mechanisms are primary Cr(VI) targets.
2018-01-01 | GSE104565 | GEO
Project description:Hexavalent chromium compounds are well-established respiratory carcinogens utilized in industrial processes. While inhalation exposure constitutes an occupational risk affecting mostly chromium workers, environmental exposure from drinking water is a widespread gastrointestinal carcinogen, affecting millions of people throughout the world. Cr(VI) is genotoxic, by forming protein-Cr-DNA adducts and silencing tumor suppressor genes, but its mechanism of action at the molecular level is poorly understood. We have used FAIRE to show that Cr(VI) elicits broad changes in chromatin accessibility resulting from disruption of the binding of transcription factors CTCF and AP-1 to their cognate sites in chromatin. Here, we have used two complementary approaches to test the hypothesis that chromium perturbs chromatin organization and dynamics. DANPOS2 analyses of MNase.seq data identified several chromatin alterations induced by Cr(VI) affecting nucleosome architecture, including occupancy changes at specific genome locations; position shifts of 10 nucleotides or more; and fuzziness, or changes in signal amplitude. Using ATAC to analyze changes in chromatin accessibility, we found that Cr(VI) opened differentially accessible chromatin domains in a dose-dependent manner. These domains were enriched for the previously identified binding motifs for CTCF and AP-1, many located in promoters of differentially expressed genes. Cr(VI)-enriched CTCF sites were confirmed by ChIP.seq and, when compared with ENCODE-validated CTCF site datasets from mouse liver, correlated with evolutionarily conserved similar sites occupied in vivo. Our results show that Cr(VI) exposure promotes broad changes in chromatin accessibility and suggest that the subsequent dysregulation of transcription may result from the disruption of CTCF binding and nucleosome spacing, suggesting that transcription regulatory mechanisms are primary Cr(VI) targets.
2018-01-01 | GSE104564 | GEO
Project description:Hexavalent chromium compounds are well-established respiratory carcinogens utilized in industrial processes. While inhalation exposure constitutes an occupational risk affecting mostly chromium workers, environmental exposure from drinking water is a widespread gastrointestinal carcinogen, affecting millions of people throughout the world. Cr(VI) is genotoxic, by forming protein-Cr-DNA adducts and silencing tumor suppressor genes, but its mechanism of action at the molecular level is poorly understood. We have used FAIRE to show that Cr(VI) elicits broad changes in chromatin accessibility resulting from disruption of the binding of transcription factors CTCF and AP-1 to their cognate sites in chromatin. Here, we have used two complementary approaches to test the hypothesis that chromium perturbs chromatin organization and dynamics. DANPOS2 analyses of MNase.seq data identified several chromatin alterations induced by Cr(VI) affecting nucleosome architecture, including occupancy changes at specific genome locations; position shifts of 10 nucleotides or more; and fuzziness, or changes in signal amplitude. Using ATAC to analyze changes in chromatin accessibility, we found that Cr(VI) opened differentially accessible chromatin domains in a dose-dependent manner. These domains were enriched for the previously identified binding motifs for CTCF and AP-1, many located in promoters of differentially expressed genes. Cr(VI)-enriched CTCF sites were confirmed by ChIP.seq and, when compared with ENCODE-validated CTCF site datasets from mouse liver, correlated with evolutionarily conserved similar sites occupied in vivo. Our results show that Cr(VI) exposure promotes broad changes in chromatin accessibility and suggest that the subsequent dysregulation of transcription may result from the disruption of CTCF binding and nucleosome spacing, suggesting that transcription regulatory mechanisms are primary Cr(VI) targets.
2018-01-01 | GSE104563 | GEO
Project description:Transcriptomic data to assess hexavalent chromium mode of action in mice and rats
| PRJNA344325 | ENA