scholarly journals Chloracne and Hyperpigmentation Caused by Exposure to Hazardous Aryl Hydrocarbon Receptor Ligands

2019 ◽  
Vol 16 (23) ◽  
pp. 4864 ◽  
Author(s):  
Masutaka Furue ◽  
Gaku Tsuji
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Environmental Pollutants ◽  
Terminal Differentiation ◽  
Keratinocyte Differentiation ◽  
Receptor Ligands ◽  
High Concentration ◽  
Skin Cells ◽  
Aryl Hydrocarbon ◽  
Antioxidative Agents ◽  
Pm2.5 Exposure

Dioxins and dioxin-like compounds are environmental pollutants that are hazardous to human skin. They can be present in contaminated soil, water, and air particles (such as ambient PM2.5). Exposure to a high concentration of dioxins induces chloracne and hyperpigmentation. These chemicals exert their toxic effects by activating the aryl hydrocarbon receptor (AHR) which is abundantly expressed in skin cells, such as keratinocytes, sebocytes, and melanocytes. Ligation of AHR by dioxins induces exaggerated acceleration of epidermal terminal differentiation (keratinization) and converts sebocytes toward keratinocyte differentiation, which results in chloracne formation. AHR activation potently upregulates melanogenesis in melanocytes by upregulating the expression of melanogenic enzymes, which results in hyperpigmentation. Because AHR-mediated oxidative stress contributes to these hazardous effects, antioxidative agents may be potentially therapeutic for chloracne and hyperpigmentation.

Analysis of aryl hydrocarbon receptor ligands in kraft mill effluents by a combination of yeast bioassays and CG-MS chemical determinations

2013 ◽  
Vol 48 (2) ◽  
pp. 145-151 ◽  
Author(s):  
Soledad Chamorro ◽  
Elizabeth Monsalvez ◽  
Benjamín Piña ◽  
Alba Olivares ◽  
Víctor Hernández ◽  
...  
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Receptor Ligands ◽  
Aryl Hydrocarbon ◽  
Kraft Mill

scholarly journals Expression, Localization, and Activity of the Aryl Hydrocarbon Receptor in the Human Placenta

2018 ◽  
Vol 19 (12) ◽  
pp. 3762 ◽  
Author(s):  
Anaïs Wakx ◽  
Margaux Nedder ◽  
Céline Tomkiewicz-Raulet ◽  
Jessica Dalmasso ◽  
Audrey Chissey ◽  
...  
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Human Placenta ◽  
Target Genes ◽  
Environmental Pollutants ◽  
Cell Fractionation ◽  
Protein Levels ◽  
Aryl Hydrocarbon ◽  
Epithelial Barriers ◽  
Expression And Activity

The human placenta is an organ between the blood of the mother and the fetus, which is essential for fetal development. It also plays a role as a selective barrier against environmental pollutants that may bypass epithelial barriers and reach the placenta, with implications for the outcome of pregnancy. The aryl hydrocarbon receptor (AhR) is one of the most important environmental-sensor transcription factors and mediates the metabolism of a wide variety of xenobiotics. Nevertheless, the identification of dietary and endogenous ligands of AhR suggest that it may also fulfil physiological functions with which pollutants may interfere. Placental AhR expression and activity is largely unknown. We established the cartography of AhR expression at transcript and protein levels, its cellular distribution, and its transcriptional activity toward the expression of its main target genes. We studied the profile of AhR expression and activity during different pregnancy periods, during trophoblasts differentiation in vitro, and in a trophoblast cell line. Using diverse methods, such as cell fractionation and immunofluorescence microscopy, we found a constitutive nuclear localization of AhR in every placental model, in the absence of any voluntarily-added exogenous activator. Our data suggest an intrinsic activation of AhR due to the presence of endogenous placental ligands.

Reduction of CC-chemokine ligand 5 by aryl hydrocarbon receptor ligands

2013 ◽  
Vol 72 (1) ◽  
pp. 9-15 ◽  
Author(s):  
Saori Morino-Koga ◽  
Hiroshi Uchi ◽  
Gaku Tsuji ◽  
Masakazu Takahara ◽  
Junboku Kajiwara ◽  
...  
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Receptor Ligands ◽  
Cc Chemokine ◽  
Aryl Hydrocarbon ◽  
Chemokine Ligand

Influence of cellular redox environment on aryl hydrocarbon receptor ligands induced melanogenesis

2021 ◽  
pp. 105282
Author(s):  
Ali Ghaffarian-Bahraman ◽  
Mohammad-Reza Arabnezhad ◽  
Majid Keshavarzi ◽  
Dorna Davani-Davari ◽  
Akram Jamshidzadeh ◽  
...  
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Receptor Ligands ◽  
Cellular Redox ◽  
Redox Environment ◽  
Aryl Hydrocarbon ◽  
Cellular Redox Environment

scholarly journals A Protective Role of Aryl Hydrocarbon Receptor Repressor in Inflammation and Tumor Growth

Cancers ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 589 ◽  
Author(s):  
Christoph F. A. Vogel ◽  
Yasuhiro Ishihara ◽  
Claire E. Campbell ◽  
Sarah Y. Kado ◽  
Aimy Nguyen-Chi ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Aryl Hydrocarbon Receptor ◽  
Inflammatory Responses ◽  
Environmental Pollutants ◽  
Protective Role ◽  
Potential Therapeutic Target ◽  
Embryonic Fibroblasts ◽  
Aryl Hydrocarbon ◽  
Enhancer Binding Protein

The aryl hydrocarbon receptor (AhR) is known for mediating the toxicity of environmental pollutants such as dioxins and numerous dioxin-like compounds, and is associated with the promotion of various malignancies, including lymphoma. The aryl hydrocarbon receptor repressor (AhRR), a ligand-independent, transcriptionally inactive AhR-like protein is known to repress AhR signaling through its ability to compete with the AhR for dimerization with the AhR nuclear translocator (ARNT). While AhRR effectively blocks AhR signaling, several aspects of the mechanism of AhRR’s functions are poorly understood, including suppression of inflammatory responses and its putative role as a tumor suppressor. In a transgenic mouse that overexpresses AhRR (AhRR Tg) we discovered that these mice suppress 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)- and inflammation-induced tumor growth after subcutaneous challenge of EL4 lymphoma cells. Using mouse embryonic fibroblasts (MEF) we found that AhRR overexpression suppresses the AhR-mediated anti-apoptotic response. The AhRR-mediated inhibition of apoptotic resistance was associated with a suppressed expression of interleukin (IL)-1β and cyclooxygenase (COX)-2, which was dependent on activation of protein kinase A (PKA) and the CAAT-enhancer-binding protein beta (C/EBPβ). These results provide mechanistic insights into the role of the AhRR to suppress inflammation and highlight the AhRR as a potential therapeutic target to suppress tumor growth.

Aryl Hydrocarbon Receptor Ligands Inhibit TGF² Induced Myofibroblast Differentiation

2012 ◽  
Author(s):  
Robert M. Kottmann ◽  
Thomas H. Thatcher ◽  
Elizabeth Lyda ◽  
Amali Epa ◽  
Richard P. Phipps ◽  
...  
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Myofibroblast Differentiation ◽  
Receptor Ligands ◽  
Aryl Hydrocarbon

Benzotriazole Ultraviolet Stabilizers Show Potent Activities as Human Aryl Hydrocarbon Receptor Ligands

2014 ◽  
Vol 49 (1) ◽  
pp. 578-587 ◽  
Author(s):  
Haruna Nagayoshi ◽  
Kensaku Kakimoto ◽  
Sokichi Takagi ◽  
Yoshimasa Konishi ◽  
Keiji Kajimura ◽  
...  
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Receptor Ligands ◽  
Aryl Hydrocarbon

The effect of benzo[α]pyrene on expression and signaling cross talk of aryl hydrocarbon receptor and NFATc1 in mouse lung tissue

2014 ◽  
Vol 32 (7) ◽  
pp. 1246-1253 ◽  
Author(s):  
Maliheh Parsa ◽  
Seyed Nasser Ostad ◽  
Seyed Mohammad Hossein Noori Moogahi ◽  
Mohammad Bayat ◽  
Mohammad Hossein Ghahremani
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Lung Tissue ◽  
Cross Talk ◽  
Environmental Pollutants ◽  
Lung Damage ◽  
Mouse Lung ◽  
Aryl Hydrocarbon ◽  
Embedded Blocks ◽  
Mouse Lung Tissue ◽  
Imagej Software

Objective: Polycyclic aromatic hydrocarbons (PAHs) are potent environmental pollutants. Benzo[α]pyrene (B[α]P) is the major compound of PAHs that acts by activating aryl hydrocarbon receptor (AhR) in cells. B[α]P is a known carcinogen and an immunotoxicant; however, its role with regard to nuclear factor of activated T cell (NFAT) pathway is unclear. AhR and NFAT signaling pathways have common roles in pathological functions in immunotoxicity and lung cancer. In this study, the effect of AhR activation on expression and signaling cross talk of AhR and NFATc1 pathways in mouse lung tissue has been investigated. Methods: Swiss albino mice were randomly allocated to five groups and administered with cyclosporin A (CsA) and B[α]P for seven constitutive days. Animals were then killed, and lung tissues were obtained after washing the whole blood. Paraffin-embedded blocks were prepared, and 5 µm sections were cut for histopathological and immunohistochemical assessments. The results were scored by observer and digitally analyzed using ImageJ software. Results: Our data showed that CsA administration resulted in a significant reduction of AhR expression. This effect was partly blocked in mice coadministrated with B[α]P and CsA. NFATc1 expression was also reduced in CsA-treated animals. Furthermore, CsA inhibited the pathological effects of B[α]P in mouse lung tissue. Conclusion: AhR expression is dependent on NFATc1 activation, and NFATc1 inhibition remarkably decreases AhR expression. However, it seems that total expression of NFATc1 is not dependent on AhR expression or activation. Moreover, CsA can prevent B[α]P-induced lung tissue damage, and it remarkably decreases NFATc1 expression. The results from this study point toward the molecular interactions of AhR and NFATc1 activation in lung tissue and the benefit of CsA treatment in B[α]P-induced lung damage.

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