The estrogenic activity of triclosan
Ontology highlight
ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE89321 | GEO | 2017/08/13
SECONDARY ACCESSION(S): PRJNA351789
REPOSITORIES: GEO
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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 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: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 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: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: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:Infections associated with antimicrobial-resistant bacteria now represent a significant threat to human health using conventional therapy, necessitating the development of alternate and more effective antibacterial compounds. Silver nanoparticles (Ag NPs) have been proposed as potential antimicrobial agents to combat infections. A complete understanding of their antimicrobial activity is required before these molecules can be used in therapy. Lysozyme coated Ag NPs were synthesized and characterized by TEMEDS, XRD, UV-vis, FTIR spectroscopy, zeta potential, and oxidative potential assay. Biochemical assays and deep level transcriptional analysis using RNA sequencing were used to decipher how Ag NPs exert their antibacterial action against multi-drug resistant Klebsiella pneumoniae MGH78578. RNAseq data revealed that Ag NPs induced a triclosan-like bactericidal mechanism responsible for the inhibition of the type II fatty acid biosynthesis. Additionally, released AgC generated oxidative stress both extra and intracellularly in K. pneumoniae. The data showed that triclosan-like activity and oxidative stress cumulatively underpinned the antibacterial activity of Ag NPs. This result was confirmed by the analysis of the bactericidal effect of Ag NPs against the isogenic K. pneumoniae MGH78578 1soxS mutant, which exhibits a compromised oxidative stress response compared to the wild type. Silver nanoparticles induce a triclosan like antibacterial action mechanism in multi-drug resistant K. pneumoniae. This study extends our understanding of anti-Klebsiella mechanisms associated with exposure to Ag NPs. This allowed us to model how bacteria might develop resistance against silver nanoparticles, should the latter be used in therapy.
2021-01-31 | GSE151953 | 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.
2010-05-19 | GSE16189 | GEO
Project description:Triclosan (TCS) is an antimicrobial toxicant found in a myriad of consumer products and has been detected in human tissues, including breastmilk. We have evaluated the impact of lactational TCS on UDP-glucuronosyltransferase 1A1 (UGT1A1) expression and bilirubin metabolism in humanized UGT1 (hUGT1) neonatal mice. In hUGT1 mice, expression of the hepatic UGT1A1 gene is developmentally delayed resulting in elevated total serum bilirubin (TSB) levels. We found that newborn hUGT1 mice breastfed or orally treated with TCS presented lower TSB levels along with induction of hepatic UGT1A1. Lactational and oral treatment by gavage with TCS leads to the activation of hepatic nuclear receptors CAR, PPARα, and stress sensor, ATF4. When CAR-deficient hUGT1 mice (hUGT1/Car-/-) were treated with TCS, TSB levels were reduced with a robust induction of hepatic UGT1A1, leaving us to conclude that CAR is not tied to UGT1A1 induction. Alternatively, when PPAR-deficient hUGT1 mice (hUGT1/Ppar-/-) were treated with TCS, hepatic UGT1A1 was not induced. Additionally, we had previously demonstrated that TCS is a potent inducer of ATF4, a transcriptional factor linked to the integrated stress response. When ATF4 was deleted in liver of hUGT1 mice (hUGT1/Atf4∆Hep), and these mice treated with TCS, we observed superinduction of hepatic UGT1A1. Oxidative stress genes in livers of hUGT1/Atf4∆Hep treated with TCS were increased, suggesting that ATF4 protects liver from excessive oxidative stress. The increase oxidative stress may be associated with superinduction of UGT1A1. The expression of ATF4 in neonatal hUGT1 hepatic tissue may play a role in the developmental repression of UGT1A1.
2024-04-24 | GSE264293 | 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.
2013-10-15 | GSE39343 | GEO