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Evaluation of Food and Food Contaminants
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
Experimental evidence demonstrates that most toxic actions of TCDD are mediated through the AhR, which is a ligand-activated transcription factor393 ubiquitously expressed in many human tissues and cell lines.394–396 AhR is inactive and unbound in the cytoplasm. Upon ligand binding, the AhR binds to the aryl hydrocarbon nuclear translocator (ARNT) protein, resulting in translocation to the nucleus, where the ligand–AhR–ARNT complex binds to response elements in the promoter of AhR-regulated genes (dioxin response element).
Serum microRNA profiles among dioxin exposed veterans with monoclonal gammopathy of undetermined significance
Published in Journal of Toxicology and Environmental Health, Part A, 2020
Weixin Wang, Youn K. Shim, Joel E. Michalek, Emily Barber, Layla M. Saleh, Byeong Yeob Choi, Chen-Pin Wang, Norma Ketchum, Rene Costello, Gerald E. Marti, Robert F. Vogt, Ola Landgren, Katherine R. Calvo
The biologic effects of TCDD are mediated through the aryl hydrocarbon receptor (AhR) which is required for optimal B-cell proliferation (Villa et al. 2017) and is involved in many critical intracellular signaling pathways. TCDD is known to induce AhR expression and activation, which in turn regulates expression of several genes affecting B-cell proliferation and survival, such as CD27, HIC1, and MTSS1 L (Kovalova et al. 2017). Dysregulation of AhR may contribute to events such as tumor initiation, promotion, and progression (Feng, Cao, and Wang 2013). In particular, Wang et al. (2019) using mouse models demonstrated that TCDD induces blood cell abnormalities and plasma cell neoplasms resembling multiple myeloma. In the Vk*Myc mouse, TCDD induced Akt and p53 phosphorylation and activation in both the spleen and bone marrow, and p53 target genes encoding Puma and p21 were upregulated by TCDD treatment (Wang et al. 2019). Further, wild-type C57BL/6 J mice exposed to TCDD developed monoclonal IgG bands analogous to MGUS.
Xenobiotic metabolism and transport in Caenorhabditis elegans
Published in Journal of Toxicology and Environmental Health, Part B, 2021
Jessica H. Hartman, Samuel J. Widmayer, Christina M. Bergemann, Dillon E. King, Katherine S. Morton, Riccardo F. Romersi, Laura E. Jameson, Maxwell C. K. Leung, Erik C. Andersen, Stefan Taubert, Joel N. Meyer
In addition to NHRs, mammalian cyp and ugt genes are regulated by the aryl hydrocarbon receptor (AHR) in response to xenobiotics, especially aromatic (aryl) hydrocarbons including polycyclic aromatic hydrocarbons, dioxins, and polychlorinated biphenyls for which AHR is an important sensor (Bock 2014; Nebert et al. 2004). The C. elegans genome also encodes an AHR gene, ahr-1, as well as a gene encoding its obligate partner, the AHR nuclear translocator (ARNT) aha-1 (Powell-Coffman, Bradfield, and Wood 1998). However, whereas mammalian AHR directly binds several aromatic xenobiotic compounds, C. elegans ahr-1 does not bind the classical AHR ligand, dioxin (Powell-Coffman, Bradfield, and Wood 1998). Further, most functional investigations on ahr-1 to date suggested that it is predominantly involved in development, especially of the nervous system (Huang, Powell-Coffman, and Jin 2004; Zhang et al. 2013). Similarly, transcriptome analyses in two ahr-1 mutants revealed a gene program largely pertinent to neuronal function and development (Aarnio et al. 2014), although some genes identified as ahr-1 dependent did feature regulatory elements annotated as xenobiotic responsive elements (XREs). Recently Brinkmann et al. (2019) suggested that ahr-1 may modulate life span in C. elegans, perhaps by modulating the effects of metabolites from commensal bacteria. In any case, the central role of mammalian AHR in the defense against certain aromatic hydrocarbons does not appear to be recapitulated by C. elegans ahr-1, and thus might arise later in evolution.
The effect of exposure to crude oil on the immune system. Health implications for people living near oil exploration activities
Published in International Journal of Environmental Health Research, 2021
Pauline McLoone, Olzhas Dyussupov, Zhaxybek Nurtlessov, Ussen Kenessariyev, Dinara Kenessary
AHR activation also seems to be important in controlling aspects of the immune response. Activation of the AHR leads to TH17 or T-regulatory cell (Treg) differentiation and IL-22 up-regulation. While IL-22 is protective against immune damage and promotes epithelial cell repair, recent studies suggest that modulation of the Treg/TH17 cell balance may be important in environmentally induced autoimmunity. Prolonged AHR binding by aromatic hydrocarbons favors differentiation of TH17 cells and can exacerbate autoimmunity (Julliard et al. 2014). Additionally, Treg cell proliferation and/or activation can hinder the immune system’s ability to clear tumors.