Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1091876 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28483834_1.fastq.gz | Fastqsanger.gz | |||
| SRR28483834_2.fastq.gz | Fastqsanger.gz | |||
| SRR28483835_1.fastq.gz | Fastqsanger.gz | |||
| SRR28483835_2.fastq.gz | Fastqsanger.gz | |||
| SRR28483836_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 18 |
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Project description:arsenic contaminated paddy soil Raw sequence reads
| PRJNA288053 | ENA
Project description:Chronic arsenic exposure can lead to various health issues including cancer. There has been a growing concern about co-exposure to various prevalent lifestyle habits and their role in the enhancement of arsenic toxicity. Smokeless tobacco (SLT) products are extensively consumed in many South Asian countries, where their use frequently co-occurs with exposure to arsenic from contaminated groundwater. To decipher the oral epithelial cell responses to arsenic and SLT alone and in co-exposure, we performed multi-omics analyses of DNA methylome, transcriptomic reprogramming and genotoxic effects in controlled experimental settings. Chronic exposure studies revealed hypomethylation of genes involved in inflammation response and apoptosis, further corroborated by the upregulation of genes involved in these processes due to arsenic and the combined treatment in acute exposure setting. Next, to validate the omics results at the phenotypic level, we observed a dose dependent decrease in cell viability, induction of DNA damage, cell cycle changes, and an increase in apoptotic cells, with the most pronounced effects observed under arsenic and SLT co-exposure conditions. The observed DNA damage was likely the result of apoptosis induction, as chronic exposure experiments based on whole-exome sequencing did not reveal increased mutagenicity following the arsenic and/or SLT exposure. Our integrative omics study provides insights into both chronic and acute responses to arsenic and SLT co-exposure, with both types of responses converging on some of the same mechanisms. We identified large-scale epigenomic and transcriptomic reprograming associated with arsenic and SLT co-exposure, alongside genotoxic effects presumably manifesting as consequences of apoptosis induction. The findings point to a role of arsenic and SLT in altering key molecular responses, especially in the context of the co-exposure, and call for further studies in humans in the areas of exposure, to validate the observed mechanisms.
2024-12-04 | GSE269688 | GEO
Project description:Chronic arsenic exposure can lead to various health issues including cancer. There has been a growing concern about co-exposure to various prevalent lifestyle habits and their role in the enhancement of arsenic toxicity. Smokeless tobacco (SLT) products are extensively consumed in many South Asian countries, where their use frequently co-occurs with exposure to arsenic from contaminated groundwater. To decipher the oral epithelial cell responses to arsenic and SLT alone and in co-exposure, we performed multi-omics analyses of DNA methylome, transcriptomic reprogramming and genotoxic effects in controlled experimental settings. Chronic exposure studies revealed hypomethylation of genes involved in inflammation response and apoptosis, further corroborated by the upregulation of genes involved in these processes due to arsenic and the combined treatment in acute exposure setting. Next, to validate the omics results at the phenotypic level, we observed a dose dependent decrease in cell viability, induction of DNA damage, cell cycle changes, and an increase in apoptotic cells, with the most pronounced effects observed under arsenic and SLT co-exposure conditions. The observed DNA damage was likely the result of apoptosis induction, as chronic exposure experiments based on whole-exome sequencing did not reveal increased mutagenicity following the arsenic and/or SLT exposure. Our integrative omics study provides insights into both chronic and acute responses to arsenic and SLT co-exposure, with both types of responses converging on some of the same mechanisms. We identified large-scale epigenomic and transcriptomic reprograming associated with arsenic and SLT co-exposure, alongside genotoxic effects presumably manifesting as consequences of apoptosis induction. The findings point to a role of arsenic and SLT in altering key molecular responses, especially in the context of the co-exposure, and call for further studies in humans in the areas of exposure, to validate the observed mechanisms.
2024-12-04 | GSE269103 | GEO
Project description:Natural or industrial pollution of source water by arsenic poses a serious threat to the health of tens of millions of people worldwide, while limited data have addressed its influence on the waterborne pathogens. This study examines the effects of arsenic exposure on Pseudomonas aeruginosa, an opportunistic pathogen that poses a health hazard in public water supplies. Our findings reveal that arsenic exposure at concentrations of 0.12–20 mg/L As(III) causes rapid growth arrest in P. aeruginosa. This exposure also leads to a marked decrease in elastase, pyocyanin, and flagellar production, while significantly increasing siderophore and extracellular polysaccharide production. Proteomic analysis indicates that both low (0.12 mg/L) and high (1.2 mg/L) arsenic levels trigger an antioxidant defense response, evidenced by the upregulation of Fnr-2, TrxB2, Ohr, AlgZ, and PslG. Concurrently, proteins related to basal metabolism, quorum sensing, T3SS, pyocyanin biosynthesis, and flagellar assembly are downregulated. Moreover, arsenic exposure enhances the expression of proteins involved in siderophore biosynthesis and transporters associated with iron uptake and multidrug resistance. In vitro assays further demonstrate that arsenic exposure reduces bacterial cytotoxicity while promoting survival and proliferation under antibiotic treatment. In summary, this study provides comprehensive insights into how arsenic affects bacterial virulence and antibiotic tolerance in P. aeruginosa, highlighting the potential public health risks posed by the frequent co-occurrence of arsenic-contaminated water sources and multidrug-resistant bacteria.
2024-08-20 | PXD055019 |