Search results for "Polychlorinated dibenzodioxins"
showing 10 items of 30 documents
Compendium of TCDD-mediated transcriptomic response datasets in mammalian model systems.
2017
Background 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is the most potent congener of the dioxin class of environmental contaminants. Exposure to TCDD causes a wide range of toxic outcomes, ranging from chloracne to acute lethality. The severity of toxicity is highly dependent on the aryl hydrocarbon receptor (AHR). Binding of TCDD to the AHR leads to changes in transcription of numerous genes. Studies evaluating the transcriptional changes brought on by TCDD may provide valuable insight into the role of the AHR in human health and disease. We therefore compiled a collection of transcriptomic datasets that can be used to aid the scientific community in better understanding the transcriptiona…
Immunologic findings in workers formerly exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin and its congeners
1998
One hundred ninety-two workers in a German pesticide factory who were exposed to polychlorinated dibenzodioxins and -furans (PCDD/PCDF) were investigated for former and present diseases and laboratory changes of the immune system. Moreover, in a subgroup of 29 highly exposed and 28 control persons, proliferation studies were performed. In addition to assays such as blood count, immunoglobulins, serum electrophoresis, monoclonal bands, surface markers, autoantibodies, and lymphocyte proliferation, two new methods, the rise of tetanus antibody concentration after vaccination and the in vitro resistance of lymphocytes to chromate, were used to diagnose the morphologic and functional state of t…
Dietary exposure and risk assessment of polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans and dioxin-like polychlorinated biphenyls of…
2018
Dietary exposure of the Valencia Region population to polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs) and PCBs was assessed in the Region of Valencia in 2010–2011. A total of 7700 food samples were collected. Occurrence data were combined with consumption data to estimate dietary exposure in adults (>15 years of age) and young people (6–15 years of age). The estimated intake was calculated by a probabilistic approach. Average intake levels (upper-bound scenario) were 1.58 and 2.76 pg toxic equivalent (TEQ) kg−1 body weight (bw) day−1 for adults and young people, respectively. These average intakes are within range of the tolerable daily intake of 1–4 pg W…
Chronic exposure of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induces an obesogenic effect in C57BL/6J mice fed a high fat diet
2017
IF 3.582; International audience; Contaminant involvement in the pathophysiology of obesity is widely recognized. It has been shown that low dose and chronic exposure to endocrine disruptor compounds (EDCs) potentiated diet- induced obesity. High and acute exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a persistent organic pollutant (POP) and an EDC with anti-estrogenic property, causes wasting syndrome . However at lower doses, the TCDD metabolic effects remain poorly understood. We investigated the obesogenic effect during chronic exposure of TCDD at 1μg/kg body weight (bw)/week in adult C57BL/6J mice fed with a high fat diet (HFD) and exposed from 10 to 42 weeks old to TCDD or e…
TCDD deregulates contact inhibition in rat liver oval cells via Ah receptor, JunD and cyclin A.
2007
The aryl hydrocarbon receptor (AhR) is a transcription factor involved in physiological processes, but also mediates most, if not all, toxic responses to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Activation of the AhR by TCDD leads to its dimerization with aryl hydrocarbon nuclear translocator (ARNT) and transcriptional activation of several phase I and II metabolizing enzymes. However, this classical signalling pathway so far failed to explain the pleiotropic hazardous effects of TCDD, such as developmental toxicity and tumour promotion. Thus, there is an urgent need to define genetic programmes orchestrated by AhR to unravel its role in physiology and toxicology. Here we show that TCDD …
TCDD-dependent downregulation of gamma-catenin in rat liver epithelial cells (WB-F344).
2002
TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) is the most potent tumor promoter ever tested in rodents. Although it is known that most of the effects of TCDD are mediated by binding to the aryl hydrocarbon receptor (AHR), the mechanisms leading to tumor promotion still remain to be elucidated. Loss of contact-inhibition is a characteristic hallmark in tumorigenesis. In WB-F344 cells, TCDD induces a release from contact-inhibition manifested by a 2- to 3-fold increase in DNA-synthesis and the emergence of foci when TCDD (1 nM) is given to confluent cells. We focussed our interest on potential cell membrane proteins mediating contact-inhibition in WB-F344 cells, namely E-cadherin, alpha,- beta,-…
Determination of 2,3,7,8-tetrachlorodibenzo-p-dioxin in goat milk and tissues by glass capillary gas chromatography and medium resolution mass fragme…
1981
Abstract An analytical method has been developed for the study of the elimination of 2,3,7,8-tetrachlodoribenzo-p-dioxin (TCDD) by lactation and its determination in various tissues of goat. The method is based on the alkaline hydrolysis of milk, liver, fat, muscle, blood, faeces and urine samples, extraction with n-hexane, treatment with sulphuric acid-saturated silica gel, chromatographic clean-up on silica gel and alumina micro-columns, and glass capillary gas chromatography—medium resolution mass fragmenography (resolution 2000). 1,2,3,4-Tetrachlorodibenzo-p-dioxin is used as the internal standard, the concentration of TCDD being determined from the calibration curve calculated from the…
Aryl hydrocarbon receptor activation by cAMP vs. dioxin: divergent signaling pathways.
2005
Even before the first vertebrates appeared on our planet, the aryl hydrocarbon receptor ( AHR ) gene was present to carry out one or more critical life functions. The vertebrate AHR then evolved to take on functions of detecting and responding to certain classes of environmental toxicants. These environmental pollutants include polycyclic aromatic hydrocarbons (e.g., benzo[ a ]pyrene), polyhalogenated hydrocarbons, dibenzofurans, and the most potent small-molecular-weight toxicant known, 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD or dioxin). After binding of these ligands, the activated AHR translocates rapidly from the cytosol to the nucleus, where it forms a heterodimer with aryl hydroc…
Uptake rates of semipermeable membrane devices (SPMDs) for PCDDs, PCDFs and PCBs in water and sediment.
2000
Uptake rates of several PCDDs, PCDFs and PCBs were measured for semipermeable membrane devices (SPMDs) under controlled conditions in bulk water and sediment. The study was performed at 19 degrees C and 11 degrees C, and water and sediment concentrations were measured during the exposure. Linear uptake rates for specific PCDD/Fs and PCBs in 19 degrees C water varied from 34 to 111 l/m2 day and in 11 degrees C water from 8.8 to 96 l/m2 day for the whole SPMD. Uptake rates at 19 degrees C sediment ranged from 9.0 to 80 mgOC/m2 day and in 11 degrees C sediment, from 3.0 to 31, mgOC/m2 day. Partitioning of the compounds between membrane and lipid was also measured during the linear uptake phase…
Degradation half-life times of PCDDs, PCDFs and PCBs for environmental fate modeling.
2000
Literature search of the knowledge on the degradation of persistent organic pollutants (POPs) in environmental compartments air, water, soil and sediment was done in purpose to find properties of POPs of interest for modeling. One degradation process, hydrolysis (chemical degradation), was omitted as negligibly slow for POPs studied. The other two, photolysis and biodegradation processes, were considered separately in purpose to develop estimation procedures. The estimates can be given as pseudo first-order rate constants kP for photolysis and kB for biodegradation. For each compartment, an overall degradation rate is k(tot) = kP + kB and lifetime t(1/2) = ln 2/k(tot). The latter values, li…