Differential DNA methylation following developmental exposure to triclosan (TCS) in 7dpf zebrafish larvae
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ABSTRACT:
PROVIDER: PRJNA415302 | ENA |
REPOSITORIES: ENA
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Project description:There is increasing evidences that toxicant exposure can alter methylation profiles, particularly during embryogenesis when DNA methylation patterns are established. In order to investigate the effects of TCS on DNA methylation and its consequences on gene expression during embryogenesis, we exposed zebrafish eggs during 7 days post fertilisation (dpf) to 50 and 100 µg/L of TCS. Although, global DNA methylation was not affected by TCS exposure, a total of 171 differentially methylated fragments (DMFs) between conditions were identified. The majority of the DMFs were found between the two exposed groups, reflecting distinct triggered responses. Gene ontology analysis revealed that pathways involved in TGF-beta signaling were enriched in larvae exposed to 50 µg/L, while de novo pyrimidine biosynthesis functions were overrepresented in fish exposed to 100 µg/L of TCS. In parallel, gene expression analysis revealed a positive correlation between DNA methylation patterns and gene expression levels for introns, together with significant alterations of the transcription of genes involved in nervous system development, transcriptional factors and histone methyltransferase. Overall our work provides evidence that TCS impacts DNA methylation during zebrafish early embryogenesis and brings clues about the toxicity mechanisms of TCS during this critical period of development.
2019-10-22 | GSE105766 | GEO
Project description:We employed whole-genome microarray expression profiling in 48 hpf zebrafish to better understand the mechanism of action of the antimicrobial agent, triclosan (TCS)
2016-10-31 | GSE80955 | GEO
Project description:Triclosan is a commonly used antibacterial and antifungal agent. However, safety of TCS has been disputed. We performed gene expression profiling of TCS and estrogen-administrered rat uterus to compare genes and cellular processes to find the effects of TCS and estrogen.
2017-08-13 | GSE89321 | GEO
Project description:Aiming at the development of a micropollutant biosensor in the frame of the Micro-Ecological Life Support System Alternative (MELiSSA), a pilot study was initiated to identify triclosan (TCS)-responsive biomarker genes in the MELiSSA carbon-mineralizing microorganism, Rhodospirillum rubrum S1H. TCS is a biocide, commonly found in human excrements and is considered an emerging pollutant in wastewater and the environment. Chronic exposure to MELiSSA-relevant concentrations (≥25 µg L-1) TCS caused a significant extension of the lag phase without affecting the growth rate. Analytical determination gave no indication of TCS biodegradation during the growth experiment and flow cytometric viability analyses revealed that TCS is only slightly toxic to R. rubrum. Through microarray analyses, the genetic mechanisms supporting the reversibility of TCS-induced inhibition were scrutinized. Hence, an extremely TCS-responsive cluster of four small adjacent genes was revealed, with up to 34-fold induction at 25 µg L-1. These four genes, for which the name micropollutant-upregulated factor (muf) was proposed; appear to be unique to R. rubrum and are shown for the first time to be involved in the response to stress. Moreover, numerous other systems that are associated with the proton-motive force were shown to be responsive to TCS, but never as highly upregulated as the muf genes. Hence, R. rubrum induced the phage shock protein operon (pspABC), numerous major facilitator efflux systems, cell envelope consolidation mechanisms, oxidative stress response, beta-oxidation, and carbonic anhydrase; while downregulating bacterial conjugation- and carboxysome synthesis genes. The muf genes and three efflux-related genes showed most potential as low-dose biomarkers. The two microarray experiments (10 and 25 µg l-1 Triclosan) were all performed in biological triplicate and containing three (in-slide) technical repeats. For all conditions, the Triclosan exposed sample (Cy5) was compared with the non-exposed solvent control (Cy3) to identify those genes that were differentially expressed upon Triclosan exposure.
2010-05-19 | E-GEOD-16189 | biostudies-arrayexpress
Project description:Triclosan (TCS), an antibacterial compound commonly added to personal care products, could be an endocrine disruptor at low doses. Although TCS has been shown to alter fetal physiology, its effects in the developing fetal brain are unknown. The objective of this study was to use transcriptomics and systems analysis to determine significantly altered biological processes in the late gestation ovine fetal hypothalamus after direct or indirect exposure to low doses of TCS. We found that short-term infusion of TCS induces vigorous changes in the fetal hypothalamic transcriptomics, which are mainly related to food intake pathways and metabolism. For direct TCS exposure, chronically catheterized late gestation fetal sheep were infused with vehicle (n=4) or TCS (250 μg/day; n=4) iv. For indirect TCS exposure, TCS (100 μg/kg/day; n=3) or vehicle (n=3) was infused into the maternal circulation. Fetal hypothalami were collected after 2 days of infusion, and gene expression was measured using Agilent 15k ovine microarrays.
2016-02-29 | E-GEOD-69275 | biostudies-arrayexpress
Project description:Triclosan (TCS), an antibacterial compound commonly added to personal care products, could be an endocrine disruptor at low doses. Although TCS has been shown to alter fetal physiology, its effects in the developing fetal brain are unknown. The objective of this study was to use transcriptomics and systems analysis to determine significantly altered biological processes in the late gestation ovine fetal hypothalamus after direct or indirect exposure to low doses of TCS. We found that short-term infusion of TCS induces vigorous changes in the fetal hypothalamic transcriptomics, which are mainly related to food intake pathways and metabolism.
2016-02-29 | GSE69275 | GEO
Project description:Triclosan (TCS), an antimicrobial agent in thousands of consumer products, is a risk factor for colitis and colitis-associated colorectal cancer. While the intestinal toxicities of TCS require the presence of gut microbiota, the molecular mechanisms involved have not been defined. Here we show that intestinal commensal microbes mediate metabolic activation of TCS in the colon and drive its gut toxicology. Using a range of in vitro, ex vivo, and in vivo approaches, we identify specific microbial β-glucuronidase (GUS) enzymes involved and pinpoint molecular motifs required to metabolically activate TCS in the gut. Finally, we show that targeted inhibition of bacterial GUS enzymes abolishes the colitis-promoting effects of TCS, supporting the essential roles of specific microbial proteins in TCS toxicity. Our results define a mechanism by which intestinal microbes cause the gut toxicity of environmental chemicals and suggest a therapeutic approach to alleviate colitis and associated diseases.
2021-11-04 | PXD025887 | Pride
Project description:In this study, the effects of Triclosan (TCS) and its alternatives, including Benzalkonium chloride (BAM), Benzethonium chloride (BEC), Chloroxylenol (CEO), Chlorhexidine (CHX) and Cetylpyridinium chloride (CPC), were investigated in THP-1 macrophages. For this purpose, untargeted proteomics was applied.
2024-02-05 | PXD044828 | Pride
Project description:Triclosan is a biocidal active agent commonly found in domestic cleaning products, hand sanitizers, cosmetics and personal care products. It is used to control microbial contamination and has a broad-spectrum of activity against many Gram-positive and Gram-negative bacteria. The development of triclosan tolerance with potential cross resistance to clinically relevant antibiotics in zoonotic pathogens is of concern given the widespread use of this active agent in clinical, food processing and domestic environments. Some studies have proposed that an over-dependence on triclosan-containing products could lead to the emergence of clinically important pathogens that are highly tolerant to both biocides and antibiotics. Currently, there is limited understanding of the mechanisms contributing to the emergence of triclosan tolerance in foodborne pathogens at a genetic level. We used microarray analysis to compare gene expression between a wildtype E. coli O157:H19 isolate (WT) with a minimum inhibitory concentration (MIC) to triclosan of 6.25 ug/ml and its laboratory generated triclosan tolerant mutant (M) with a MIC of >8000 ug/ml.
2013-10-15 | GSE39343 | GEO
Project description:Triclosan is a biocidal active agent commonly found in domestic cleaning products, hand sanitizers, cosmetics and personal care products. It is used to control microbial contamination and has a broad-spectrum of activity against many Gram-positive and Gram-negative bacteria. The development of triclosan tolerance with potential cross resistance to clinically relevant antibiotics in zoonotic pathogens is of concern given the widespread use of this active agent in clinical, food processing and domestic environments. Some studies have proposed that an over-dependence on triclosan-containing products could lead to the emergence of clinically important pathogens that are highly tolerant to both biocides and antibiotics. Currently, there is limited understanding of the mechanisms contributing to the emergence of triclosan tolerance in foodborne pathogens at a genetic level. We used microarray analysis to compare gene expression between a wildtype E. coli O157:H19 isolate (WT) with a minimum inhibitory concentration (MIC) to triclosan of 6.25 ug/ml and its laboratory generated triclosan tolerant mutant (M) with a MIC of >8000 ug/ml. Gene expression profiling was performed on untreated E. coli O157:H19 wildtype (WTu) and mutant (Mu), and on the wildtype and mutant treated with 6 ug/ml triclosan for 30 minutes (WTt and Mt respectively). RNA was extracted from three independent biological replicates for WTu, Mu, WTt & Mt for hybridization on Affymetrix GeneChip E. coli Genome 2.0 Arrays. Micorarray analysis including pre-processing, normalisation and statistical analysis were performed using R (R, 2007) version 2.6 and Bioconductor (Gentleman et al. 2004, Genome Biol. 5:R80) version 2.1 as previously described by Morris et al.(2009, Physiol. Genomics 39:28-37).
2013-10-15 | E-GEOD-39343 | biostudies-arrayexpress