TY - JOUR. T1 - Signaling pathway for 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced TNF-α production in differentiated THP-1 human macrophages. AU - Cheon, Hyeon Joo. AU - Woo, Young Seok. AU - Ji, Young Lee. AU - Hee, Sook Kim. AU - Hyun, Jin Kim. AU - Cho, Sungwon. AU - Nam, Hee Won. AU - Sohn, Jeongwon. PY - 2007/8/31. Y1 - 2007/8/31. N2 - 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a prototypic halogenated aromatic hydrocarbon (HAH), is known as one of the most potent toxicants. At least a part of its toxic effects appears to be derived from its ability to induce TNF-α production. However, the signaling pathway of TCDD that leads to TNF-α expression has not been elucidated. In this study, we investigated the signaling mechanism of TCDD-induced TNF-α expression in PMA-differentiated THP-1 macrophages. TCDD induced both mRNA and protein expression of TNF-α in a dose- and time-dependent manner. α-Naphthoflavone (NF), an aryl hydrocarbon receptor (AhR) inhibitor, prevented the TCDD-induced ...
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a polychlorinated dibenzo-p-dioxin (sometimes shortened, though inaccurately, to simply "dioxin") with the chemical formula C 12H 4Cl 4O 2. TCDD is a colorless solid with no distinguishable odor at room temperature. It is usually formed as a side product in organic synthesis and burning of organic materials. TCDD is the most potent compound (congener) of its series (polychlorinated dibenzodioxins, known as PCDDs or simply dioxins) and became known as a contaminant in Agent Orange, a herbicide used in the Vietnam War. TCDD was released into the environment in the Seveso disaster. It is a persistent environmental contaminant usually present in a complex mixture of dioxin-like compounds, and is a carcinogen. The Expert Group of the World Health Organization considered developmental toxicity as the most pertinent risk of dioxins to human beings. Because people are usually exposed simultaneously to a number of dioxin-like chemicals, a more detailed ...
2,3,7,8 Tetrachlorodibenzo-p-dioxin (TCDD), a ubiquitous environmental toxin, has been shown to cause a human skin pathology called chloracne. The majority of laboratory mouse strains, with the exception of mice bearing a mutation in thehairless gene, fail to display overt signs of chloracne upon exposure to TCDD. As a result, only minimal data exist on the effects of TCDD in adult haired mice and no data exist on the effects of TCDD in developing mouse skin. Here we report that TCDD affects the temporal expression of protein markers of keratinocyte terminal differentiation during murine skin morphogenesis. Immunohistochemical analysis of E16 mice reveals accelerated expression of the intermediate filament-associated protein filaggrin in response to TCDD. At a later developmental time and after birth, expression of filaggrin and loricrin is indistinguishable between treatment and control groups. At E16 expression of keratins 5, 6, and 10 are unaltered in TCDD-exposed individuals and TUNEL ...
In vitro systems have inherent limitations in their ability to model whole organism gene responses, which must be identified and appropriately considered when developing predictive biomarkers of in vivo toxicity. Systematic comparison of in vitro and in vivo temporal gene expression profiles were conducted to assess the ability of Hepa1c1c7 mouse hepatoma cells to model hepatic responses in C57BL/6 mice following treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Gene expression analysis and functional gene annotation indicate that Hepa1c1c7 cells appropriately modeled the induction of xenobiotic metabolism genes in vivo. However, responses associated with cell cycle progression and proliferation were unique to Hepa1c1c7 cells, consistent with the cell cycle arrest effects of TCDD on rapidly dividing cells. In contrast, lipid metabolism and immune responses, representative of whole organism effects in vivo, were not replicated in Hepa1c1c7 cells. These results identified inherent differences in
The present study assessed if eating a diet of fish, spiked with persistent organic pollutants (POPs), affects gene and protein expression in the maturing mouse brain. Juvenile female Balb/c mice (22 days of age) were exposed for 28 days to fish-based diets spiked with the dioxin 2,3,7,8-tetrachlorodibenzodioxin (TCDD) or the non dioxin-like (NDL) chemicals hexabromocyclodocecane (HBCD), 2,24,4-tetrabromodiphenylether (BDE-47) or 2,24,4,5,5-hexachlorobiphenyl (CB-153) at doses approximating their respective lowest observed adverse effect levels (LOAEL). It was found that all POPs elicited changes in neural gene and protein expression profiles. Bioinformatic analysis of gene expression data highlighted the importance of the aryl hydrocarbon receptor (AHR) in dioxin toxicity and revealed that zinc regulation in the brain is targeted by TCDD through the AHR. Calcium homeostasis was affected by both TCDD and the NDL chemicals. In contrast to the transcriptomic analysis, the proteomics data did not
The fact that the molecular mechanisms of dioxin toxicity are still poorly understood complicates dioxin risk assessment. Only one mechanism of dioxin action, the direct induction of CYP1A1, has been elucidated in detail (5). However, despite its direct regulation by the AHR, CYP1A1 induction is not predictive of dioxin toxicity.. A useful tool for studying the mechanisms of dioxin toxicity is the large sensitivity difference in TCDD-induced lethality between H/W and L-E rat strains. Although there is a large sensitivity difference in certain endpoints of TCDD toxicity (e.g. acute lethality, wasting, and hepatotoxicity), other responses, such as induction of CYP1A1, remain similar between these strains (3). A wide range of clinical chemistry variables and biochemical parameters have been investigated in an effort to rationalize the differences between these two strains, but no clear molecular factors responsible for TCDD resistance in the H/W rat strain have been identified.. The aim of this ...
2, 3, 7, 8-Tetrachlorodibenzo-p-dioxin is well known for its immunotoxic effects on the thymus, as well as on B and T lymphocyte functions. Previous studies suggested that TCDD exerted immunotoxic effects only on cells differentiating in response to antigenic challenge. To this date, no work has been done to characterize the long-term effects of TCDD on the activated cells. Additionally, no studies have been done to determine whether TCDD has any effect on resting T cells. In the current study, therefore, we investigated the effects of TCDD on activated and resting cells within the same animal. T cells in the popliteal lymph node cells were activated by rear footpad immunizations with anti-CD3 antibodies. Distally-located axillary lymph nodes were chosen as a source of naive and resting T cells. Our results demonstrate that TCDD acted at the time of cell differentiation to suppress the immune responses of activated T cells, but failed to suppress, and at times, enhanced the immune responses of ...
Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS) and Seveso Womens Health Studies (SWHS) similarities: 1. Both are prospective cohort studies of more highly exposed populations; 2. Both use biomarkers of exposure; and, 3. Both study multiple health outcomes. CHAMACOS and SWHS differences: 1. CHAMACOS focuses on childrens health, SWHS focuses on womens health. 2. CH
2,3,7,8-Tetrachlorodibenzo-p-dioxin(TCDD) has previously shown to induce neurotoxicity through intracellular $Ca^{2+}$ increase in rat neurons. In this study we investigated the role and signaling pathway of intracellular $Ca^{2+}$ in TCDD-induced inhibition of neuronal cell proliferation in SK-...
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TY - JOUR. T1 - Ah receptor for 2,3,7,8-tetrachlorodibenzo-p-dioxin. T2 - Comparative studies in mammalian and nonmammalian species. AU - Denison, Michael S.. AU - Wilkinson, Christopher F.. AU - Okey, Allan B.. PY - 1986. Y1 - 1986. N2 - The Ah receptor was identified and characterized in cytosol from a large number of diverse animal species. Molecular properties of the Ah receptor were similar in all species which had detectable receptor. However, subtle differences in receptor properties exist among animal species and these differences indicate that the Ah receptor protein is not identical in all species. It is not yet known whether differences in receptor properties among animal species play a significant role in determining differential susceptibility of the species to toxicity from halogenated aromatic compounds.. AB - The Ah receptor was identified and characterized in cytosol from a large number of diverse animal species. Molecular properties of the Ah receptor were similar in all ...
40 Although 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) was one of the most potent environmental carcinogen, mechanisms of action of TCDD at the molecular level are poorly understood. To enhance our understanding of carcinogenicity by TCDD, we investigated which genes are involved in TCDD-induced chemical carcinogenesis using two human liver cells, hepatoma HepG2 and non-tumorigenic fetal hepatic WRL68 cells. We found that TCDD (1nM) decreased HepG2 cell growth over 50%, but had no effect on WRL68 cell growth. We used DNA microarray to identify genes whose expression are changed at 24 hours after treatment with TCDD (0.1nM) in both of cell lines. We found that TCDD commonly down-regulated P21, sod1 genes and up-regulated hsp27, hsp90 genes, two fold or more. Moreover, TCDD (0.1nM) increased the levels of 8-hydroxy-2-deoxyguanosine (8-OHdG), typical biomarker of oxidative stress, with time dependency in HepG2 cell, but just transiently increased the levels of 8-OHdG after 2 hours in WRL68 cell. ...
AhR ligands are a structurally diverse group of natural and synthetic compounds that elicit a broad range of biological effects (13, 14, 25). Here, we analyze two AhR ligands, DIM and TCDD, which have opposing effects on human and animal health. DIM is a beneficial dietary constituent that suppresses breast tumors in rodents (9, 10) and may decrease breast cancer risk in humans (6). TCDD is a highly toxic, man-made environmental contaminant that is implicated in birth defects, infertility, and cancer (14, 15, 26). We find that DIM and TCDD differ in their ability to activate the two distinct AhR-controlled pathways: transcriptional activation and hormone receptor degradation. TCDD is better than DIM at activating CYP1 expression. DIM is better than TCDD at suppressing ER-α expression and estrogen signaling. This finding, that AhR ligands can preferentially activate the distinct AhR-controlled pathways, implies that the biological effects of different AhR ligands may vary considerably. This may ...
(2012) Yao et al. Toxicology and Applied Pharmacology. The biochemical and toxic effects of 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD) have been the subject of intense study for decades. It is now clear that essentially all TCDD-induced toxicities are mediated by DNA-protein interactions involvi...
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Looking for online definition of Tetrachlorodibenzodioxin in the Medical Dictionary? Tetrachlorodibenzodioxin explanation free. What is Tetrachlorodibenzodioxin? Meaning of Tetrachlorodibenzodioxin medical term. What does Tetrachlorodibenzodioxin mean?
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), the prototypic ligand for the aryl hydrocarbon receptor (AhR), promotes tumor formation in some model systems. However, with regard to breast cancer, epidemiological and animal studies are inconclusive as to whether exposure increases tumor incidence or may instead be protective. We have previously reported that mice exposed to TCDD during pregnancy have impaired differentiation of mammary tissue, including decreased branching and poor development of lobuloalveolar structures. Because normal pregnancy-induced mammary differentiation may protect against subsequent neoplastic transformation, we hypothesized that TCDD-treated mice would be more susceptible to chemical carcinogenesis after parturition. To test this, mice were treated with TCDD or vehicle during pregnancy. Four weeks later, 7,12-dimethylbenz[a]anthracene (DMBA) was administered to induce mammary tumor formation. Contrary to our hypothesis, TCDD-exposed parous mice showed a 4-week delay in ...
The aryl hydrocarbon receptor (AhR) is a transcription factor belonging to the Per-ARNT-Sim family of proteins. These proteins sense molecules and stimuli from the cellular/tissue environment, and initiate signaling cascades to elicit appropriate cellular responses. Recent literature suggests an important function of AhR in hematopoietic stem cell (HSC) biology. However, the molecular mechanisms by which AhR signaling regulates HSC functions are unknown. In previous studies, we and others reported that treatment of mice with the AhR agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) compromises the competitive reconstitution of bone marrow (BM) cells into irradiated host animals. Additional studies indicated a requirement for AhR in hematopoietic cells and not marrow microenvironment cells. In this study, we tested the hypothesis that TCDD-mediated phenotypic and functional changes of HSCs are a result of changes in gene expression that disrupt stem cell numbers and/or their migration. TCDD ...
Looking for online definition of 2,3,7,8-tetrachlorodibenzo-p-dioxin in the Medical Dictionary? 2,3,7,8-tetrachlorodibenzo-p-dioxin explanation free. What is 2,3,7,8-tetrachlorodibenzo-p-dioxin? Meaning of 2,3,7,8-tetrachlorodibenzo-p-dioxin medical term. What does 2,3,7,8-tetrachlorodibenzo-p-dioxin mean?
TY - JOUR. T1 - Ligand-independent activation of the arylhydrocarbon receptor by ETK (Bmx) tyrosine kinase helps MCF10AT1 breast cancer cells to survive in an apoptosis-inducing environment. AU - Fujisawa, Yasuko. AU - Li, Wen. AU - Wu, Dalei. AU - Wong, Patrick. AU - Vogel, Christoph. AU - Dong, Bin. AU - Kung, Hsing Jien. AU - Matsumura, Fumio. PY - 2011/10/1. Y1 - 2011/10/1. N2 - It has been reported that the arylhydrocarbon receptor (AHR) is overexpressed in certain types of breast tumors. However, so far no concrete evidence has been provided yet as to why and how the overexpressed AHR in those cancer cells is functionally activated without exogenous ligands. Here we show that the AHR was functionally activated when estrogen receptor-negative, AHR overexpressing MCF10AT1 human breast cancer cells (designated P20E) were subjected to serum starvation. Transfection of cells with ETK-KQ, a plasmid for kinase-dead epithelial and endothelial tyrosine kinase (ETK), attenuated this AHR activation. ...
Patients with ER-negative breast tumors are among the most difficult to treat and exhibit low survival rates due, in part, to metastasis from the breast to various distal sites. Aryl hydrocarbon receptor (AHR) ligands show promise as antimetastatic drugs for estrogen receptor (ER)-negative breast cancer. Triple negative MDA-MB-231 breast cancer cells were treated with eight AHR-active pharmaceuticals including 4-hydroxtamoxifen, flutamide leflunomide, mexiletine, nimodipine, omeprazole, sulindac and tranilast, and the effects of these compounds on cell proliferation (MTT assay) and cell migration (Boyden chamber assay) were examined. The role of the AHR in mediating inhibition of MDA-MB-231 cell invasion was investigated by RNA interference (RNAi) and knockdown of AHR or cotreatment with AHR agonists. Lung metastasis of MDA-MB-231 cells was evaluated in mice administered cells by tail vein injection and prometastatic gene expression was examined by immunohistochemistry. We showed that only the proton
OBJECTIVE--The aim was to examine the long term morbidity experience of men exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). METHODS--A retrospective cohort morbidity study of 158 men first exposed to TCDD between 17 November 1953 and 16 November 1954 subdivided by chloracne state and back calculated TCDD blood lipid concentration, and 161 referents. Cause specific illness absence and admissions to hospital were examined between 1953 and 1989. RESULTS--On an ever or never basis, thyroid disease and appendicitis were diagnosed more often in the study group; these diseases were not differentially distributed by chloracne state, but were increased in the high TCDD subgroup. An 18% increase in total illness episodes was also seen (p = 0.002); illness rates increased with severity of chloracne and higher TCDD concentration within the chloracne subgroup. There were increases in infectious and parasitic diseases (primarily ill defined intestinal infections), disorders of the peripheral nervous ...
The ligand-dependent transcription factor aryl hydrocarbon receptor (AhR) has been implicated in various immune functions. Our previous studies have shown that AhR activation by exposure of ovalbumin (OVA)-immunized mice to the potent ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) increases immunization-induced IFN- production in the spleen and suppresses the production of Th2 cytokines and OVA-specific antibodies. In the present study, we used transgenic (Tg) mice that express a constitutively active mutant of aryl hydrocarbon receptor (CA-AhR) specifically in T-lineage cells to clarify the role of AhR activation in T cells in these reactions. The results of this study clearly demonstrated that AhR activation only in the T cells augments IFN- production upon OVA immunization. By contrast, production of Th2 cytokines and antibodies were not significantly suppressed by CA-AhR in the T cells. These results suggest that suppression of Th2 cytokines and antibodies production require AhR ...
Free Online Library: AhR-mediated effects of dioxin on neuronal acetylcholinesterase expression in vitro.(Research, Report) by Environmental Health Perspectives; Health, general Environmental issues Acetylcholinesterase Chlorocarbons Analysis Dibenzofurans Dichloropropane Dioxin Health aspects Dioxins Enzymes Neurons
The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that upon activation by the toxicant 2,3,7,8 tetrachlorodibenzo-p-dioxin (TCDD) stimulates gene expression and toxicity. AHR is also important for normal mouse physiology and may play a role in cancer progression in the absence of environmental toxicants. The objective of this report was to identify AHR-dependent genes (ADGs) whose expression is regulated by AHR in the absence of toxicants. RNA-Seq analysis revealed that AHR regulated the expression of over 600 genes at an FDR | 10% in MCF-7 breast cancer cells upon knockdown with short interfering RNA. Pathway analysis revealed that a significant number of ADGs were components of TCDD and tumor necrosis factor (TNF) pathways. We also demonstrated that siRNA knockdown of AHR modulated TNF induction of MNSOD and cytotoxicity in MCF-7 cells. Collectively, the major new findings of this report are: (1) endogenous AHR promotes the expression of xenobiotic metabolizing enzymes
Conclusions and implications.Currently, there are several signaling cascades that define a novel biological theme in which the interplay between nuclear export and protein degradation plays a major role in determining the magnitude and duration of gene regulation. For example, the level of p53 protein is controlled in part by nuclear export and subsequent degradation by cytoplasmic proteases (8, 14,44, 45). If nuclear export of p53 is inhibited, there is a general upregulation of p53-dependent genes (8, 37). Another pathway involves p27Kip1, p27Kip1 is a cyclin-dependent kinase that arrests cells in G1(40) and appears to be reduced in certain types of cancer (43). Importantly, the level of p27Kip1 is controlled in part through nuclear export following association with p38 (JAB1), a protein that contains an NES and allows export of p27Kip1 to the cytoplasm for degradation (27,46). The common theme in both pathways is that the export of the effector protein from the nucleus results in reduced ...
Alshahrani S, Alvarez-Leefmans FJ, Di Fulvio M. 2012. Expression of the Slc12a1 gene in pancreatic β-cells: molecular characterization and in silico analysis. Cell Physiol Biochem 30:95-112.. Alwasel SH, Ashton N. 2009. Prenatal programming of renal sodium handling in the rat. Clin Sci (Lond) 117:75-84.. Aragon AC, Kopf PG, Campen MJ, Huwe JK, Walker MK. 2008. In utero and lactational 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure: effects on fetal and adult cardiac gene expression and adult cardiac and renal morphology. Toxicol Sci 101:321-330.. Au CG, Butler TL, Sherwood MC, Egan JR, North KN, Winlaw DS. 2011. Increased connective tissue growth factor associated with cardiac fibrosis in the mdx mouse model of dystrophic cardiomyopathy. Int J Exp Pathol 92:57-65.. Barker DJ, Gluckman PD, Godfrey KM, Harding JE, Owens JA, Robinson JS. 1993. Fetal nutrition and cardiovascular disease in adult life. Lancet 341:938-941.. Barker DJ, Winter PD, Osmond C, Margetts B, Simmonds SJ. 1989. Weight in ...
GNF351 is a full aryl hydrocarbon receptor (AHR) antagonist. GNF351 competes with a photoaffinity AHR ligand for binding to the AHR with an IC50 of 62 nM. GNF351 is minimal toxicity in mouse or human keratinocytes. - Mechanism of Action & Protocol.
Aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor and its expression is influenced by environmental compounds, such as 3-methylcholanthrene (3-MC) and β-naphthoflavone (β-NF). AhR and its downstream genes, such as CYP1A1, are considered to play a pivotal role in xenobiotic responses. AhR signaling has also been proposed to mediate osteogenesis in experimental animals, but its details have remained unclear. Therefore, in this study, we examined the possible roles of AhR in human bone. Immunohistochemical analysis revealed that AhR was detected in both osteoblasts and osteoclasts. We then screened AhR-target genes using a microarray analysis in human osteoblastic hFOB cells. Results of microarray and subsequent PCR analysis did reveal that estrogen metabolizing and synthesizing enzymes, such as CYP1B1 and aromatase, were increased by 3-MC in hFOB and osteosarcoma cell line, MG-63. The subsequent antibody cytokine analysis also demonstrated that interleukin-1β and -6 expression
The aryl hydrocarbon receptor (AhR) is a cytosolic ligand-activated transcription factor that mediates most of the toxic and carcinogenic effects of drugs and environmental toxins collectively known as xenobiotics. Ligand activation of the AhR stimulates the transcription of genes that encode several xenobiotic-metabolizing enzymes. The molecular mechanisms and signaling pathways evoked by the activation of the AhR are becoming increasingly understood and underscore the participation of the AhR in crucial processes, including cellular stress response, proliferation, differentiation, inflammation, and carcinogenesis. Studies now implicate the AhR as an integral part of the multifaceted signal transduction pathway initiated by the exposure of keratinocytes to ultraviolet B radiation (UVB), which is the most ubiquitous hazard to human skin and the principal risk factor for skin cancer. Ligand-dependent activation of the AhR in the cytosol provides a molecular bridge that links cytoplasmic events to ...
4940 The arylhydrocarbon receptor (AhR) is a ligand-activated transcription factor regulating transcription of genes encoding primarily drug metabolizing enzymes. Use of its persistent agonists such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related compounds demonstrated that the AhR mediates species- and tissue-dependent toxicities, including wasting syndrome, immunotoxicty, and carcinogenesis. It has been reported that expression of a constitutively active mutant AhR in transgenic mice resulted in development of stomach tumors, demonstrating the oncogenic potentials of the AhR in gastric cancer. On the other hand, recent reports showed that AhR agonists inhibited pancreatic cancer cell growth and that AhR pathway mediated the effect of antitumor agent in breast tumor cells. To elucidate the functional significance of the AhR pathway in gastric cancer, we examined the expression of AhR in gastric cancer tissues and cell lines and the effect of AhR agonists in gastric cancer cell lines. ...
Abbott BD, Birnbaum LS. 1990. Rat embryonic palatal shelves respond to TCDD in organ-culture. Toxicol Appl Pharmacol 103(3):441-451.. Abbott BD, Held GA, Wood CR, Buckalew AR, Brown JG, Schmid J. 1999. AhR, ARNT, and CYP1A1 mRNA quantitation in cultured human embryonic palates exposed to TCDD and comparison with mouse palate in vivo and in culture. Toxicol Sci 47(1):62-75.. Abbott BD, Lin TM, Rasmussen NT, Albrecht RM, Schmid JE, Peterson RE. 2003. Lack of expression of EGF and TGF-alpha in the fetal mouse alters formation of prostatic epithelial buds and influences the response to TCDD. Toxicol Sci 76(2):427-436.. Adamsson A, Simanainen U, Viluksela M, Paranko J, Toppari J. 2009. The effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin on foetal male rat steroidogenesis. Int J Androl 32(5):575-585.. Allgeier SH, Vezina CM, Lin TM, Moore RW, Silverstone AE, Mukai M, Gavalchin J, Cooke PS, Peterson RE. 2009. Estrogen signaling is not required for prostatic bud patterning or for its disruption by ...
It has been reported that fetal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) causes defects in the male reproductive system of the rat. We set out to replicate and extend these effects using a robust experimental design. Groups of 75 (control vehicle) or 55 (50, 200 or 1000 ng of TCDD kg-1 bodyweight) female Wistar(Han) rats were exposed to TCDD on Gestational Day (GD) 15, then allowed to litter. The high dose group dams showed no sustained weight loss compared to control, but four animals had total litter loss. Pups in the high dose group showed reduced body weight up till day 21, and pups in the medium dose group showed reduced body weight in the first week post partum. Balano-preputial separation (BPS) was significantly delayed in the high dose group male offspring. There were no significant effects of treatment when the offspring were subjected to a functional observational battery, or mated with females to assess reproductive capability. 25 males per group were killed on post ...
Preface. A. Historical background.. 1. History of Research on the AHR (Thomas A. Gasiewocz and Ellen C. Henry).. B. AHR as a ligand-activated transcription factor.. 2. Overview of AHR functional domains and the classical signaling pathway: induction of drug-metabolizing enzymes (Qiang Ma).. 3. Role of chaperone proteins in AHR function (Iain A. Murray and Gary H. Perdew).. 4. AHR Ligands: Promiscuity in Binding and Diversity in Response (Danica DeGroot, Guochun He, Domenico Fraccalvieri, Laura Bonati, Allesandro Pandin and Michael S. Denison).. 5. Dioxin response elements and regulation of gene transcription (Hollie Swanson).. 6. The AHR/ARNT dimer and transcriptional coactivators (Oliver Hankinson).. 7. Regulation of AHR by the AHR repressor (AHRR) (Yoshiaki Fujii-Kuriyama and Kaname Kawajiri).. 8. Influence of HIF-1α and Nrf2 signaling on AHR-mediated gene expression, toxicity and biological functions (Thomas Haarmann-Stemmann and Josef Abel).. 9. Functional interactions of AHR with other ...
Page contains details about example of polymer-coated aryl hydrocarbon receptor transcription factor-binding ligand loaded magnetic nanoparticles . It has composition images, properties, Characterization methods, synthesis, applications and reference articles : nano.nature.com
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... , Authors: Sayka Barry, Márta Korbonits. Published in: Atlas Genet Cytogenet Oncol Haematol.
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Chrysin greatly increased UGT1A1 expression in immortalized cell lines, such as Caco-2 and HepG2 cells, in previous reports (Galijatovic et al., 2000, 2001; Walle et al., 2000). Our studies confirmed the large induction observed in HepG2 cells. However, only a few reports have focused on the mechanism by which chrysin induces drug-metabolizing enzymes. Zhang et al. (2003) found that the induction of CYP1A1 reporter activity by chrysin was mediated through AhR activation and subsequent binding to dioxin-responsive elements present in the gene in HepG2 cells. In a separate study, Sugatani et al. (2004) found that the UGT1A1 response to chrysin was alleviated the most when the AhRE within the gtPBREM was mutated in transactivation experiments conducted in HepG2 cells. UGT1A1 and CYP2B6 gene reporter activation by chrysin and 3-MC was compared in HepG2 cells in the present study. CYP2B6 was not responsive to chrysin, but it was responsive to PB, a PXR and CAR activator, when the PBREM was ...
Complete information for AHR gene (Protein Coding), Aryl Hydrocarbon Receptor, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
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Humans are exposed daily to low concentrations of many different chemical substances, natural and some man-made. Although many of these substances can be toxic at high levels, typical exposures are far below the effect levels. The responses produced by man-made aromatic hydrocarbon receptor agonists, such as dioxins, polychlorinated...
Methods 45 workers who had been exposed to high levels of TCDD in the past and 108 non-exposed workers (39 from the same factory as the exposed subjects (internal control group) and 69 from a comparable factory but without TCDD exposure (external control group)) were included in the study. Blood immunoglobulin (Ig) and complement factor (C) concentrations and specific IgE antibodies to a panel of common allergens were measured using quantitative nephelometry or ELISA. TCDD plasma levels were measured and back-extrapolated to the time of last exposure (TCDDmax) using a one-compartment first order kinetic model. ...
Neubert R, Jacob-Muller U, et al. Polyhalogenated dibenzo-p-dioxins and dibenzofurans and the immune system. 2. In vitro effects of, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on lymphocytes of venous blood from man and a non-human primate (Callithrix jacchus). Arch Toxicol. 1991;65:213-9 ...
Although the perception of dioxins is predominantly negative, they have also been shown to exert beneficial effects in animal models, such as immunostimulation, reduced cancer rates and prolongation of life at sufficiently low (hormetic) doses. Furthermore, some effects at supra-hormetic doses can be considered desirable under certain conditions. Lowering of body weight or increased insulin sensitivity could contribute to the quest for treating obesity or diabetes mellitus type II. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) binds readily to the aryl hydrocarbon receptor (AhR), and, thereby exerts many of its effects. The binding of potential drug candidates to the AhR, however, is often considered detrimental. The expected subsequent induction of CYP1A1 activity is still associated with the metabolic activation of potential carcinogens despite naturally occurring AhR agonists in food. Therefore, a separation of AhR interaction and downstream effects could lead to the exploitation of the ...
Rabbit polyclonal Aryl hydrocarbon Receptor antibody validated for WB and tested in Human and Mouse. With 2 independent reviews. Immunogen corresponding to…
The rat and hamster exhibit about a 100-fold difference in sensitivity to the acute toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), with the hamster representing the most resistant species examined to date. The present study compared the induction and inhibition of hepatic TCDD metabolism in these species using suspensions of isolated hepatocytes. Purified 14C-TCDD or 3H-TCDD (2.2 microM) was incubated for 2-6 hr with hepatocytes isolated from untreated, TCDD-pretreated (5 micrograms/kg, ip), 3-methylcholanthrene-pretreated (3-MC, 50 mg/kg, ip, x 3 days), isosafrole-pretreated (ISO, 150 mg/kg, ip, x 3 days), or phenobarbital-pretreated (PB, 80 mg/kg, ip, x 3 days) rats and hamsters. Untreated rat and hamster hepatocytes metabolized TCDD at a similar rate (0.20 and 0.18 pmol/hr/mg, respectively). In both species, TCDD and 3-MC pretreatments elevated the rate of TCDD metabolism by 5-6-fold, while PB pretreatment had no effect. isosafrole modestly increased (1.8-2.5-fold) TCDD metabolism in ...