PMID- 32354640
OWN - NLM
STAT- MEDLINE
DCOM- 20210618
LR  - 20220716
IS  - 2213-2317 (Electronic)
IS  - 2213-2317 (Linking)
VI  - 34
DP  - 2020 Jul
TI  - The aryl hydrocarbon receptor as a target of environmental stressors - 
      Implications for pollution mediated stress and inflammatory responses.
PG  - 101530
LID - S2213-2317(20)30225-1 [pii]
LID - 10.1016/j.redox.2020.101530 [doi]
LID - 101530
AB  - The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor 
      regulating the expression of genes, for instance encoding the monooxygenases 
      cytochrome P450 (CYP) 1A1 and CYP1A2, which are important enzymes in metabolism 
      of xenobiotics. The AHR is activated upon binding of polycyclic aromatic 
      hydrocarbons (PAHs), persistent organic pollutants (POPs), and related ubiquitous 
      environmental chemicals, to mediate their biological and toxic effects. In 
      addition, several endogenous and natural compounds can bind to AHR, thereby 
      modulating a variety of physiological processes. In recent years, ambient 
      particulate matter (PM) associated with traffic related air pollution (TRAP) has 
      been found to contain significant amounts of PAHs. PM containing PAHs are of 
      increasing concern as a class of agonists, which can activate the AHR. Several 
      reports show that PM and AHR-mediated induction of CYP1A1 results in excessive 
      generation of reactive oxygen species (ROS), causing oxidative stress. 
      Furthermore, exposure to PM and PAHs induce inflammatory responses and may lead 
      to chronic inflammatory diseases, including asthma, cardiovascular diseases, and 
      increased cancer risk. In this review, we summarize findings showing the critical 
      role that the AHR plays in mediating effects of environmental pollutants and 
      stressors, which pose a risk of impacting the environment and human health.
CI  - Copyright (c) 2020 The Authors. Published by Elsevier B.V. All rights reserved.
FAU - Vogel, Christoph F A
AU  - Vogel CFA
AD  - Center for Health and the Environment, University of California, One Shields 
      Avenue, Davis, CA, 95616, USA; Department of Environmental Toxicology, University 
      of California, One Shields Avenue, Davis, CA, 95616, USA.
FAU - Van Winkle, Laura S
AU  - Van Winkle LS
AD  - Center for Health and the Environment, University of California, One Shields 
      Avenue, Davis, CA, 95616, USA; School of Veterinary Medicine Department of 
      Anatomy, University of California, One Shields Avenue, Davis, CA, 5616, USA.
FAU - Esser, Charlotte
AU  - Esser C
AD  - IUF - Leibniz-Research Institute for Environmental Medicine, 40225, Dusseldorf, 
      Germany.
FAU - Haarmann-Stemmann, Thomas
AU  - Haarmann-Stemmann T
AD  - IUF - Leibniz-Research Institute for Environmental Medicine, 40225, Dusseldorf, 
      Germany. Electronic address: Thomas.haarmann-stemmann@iuf-duesseldorf.de.
LA  - eng
GR  - P30 CA093373/CA/NCI NIH HHS/United States
GR  - P30 ES023513/ES/NIEHS NIH HHS/United States
GR  - R01 ES029126/ES/NIEHS NIH HHS/United States
GR  - R21 ES030419/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20200418
PL  - Netherlands
TA  - Redox Biol
JT  - Redox biology
JID - 101605639
RN  - 0 (Particulate Matter)
RN  - 0 (Polycyclic Aromatic Hydrocarbons)
RN  - 0 (Receptors, Aryl Hydrocarbon)
SB  - IM
MH  - Gene Expression Regulation
MH  - Humans
MH  - Particulate Matter
MH  - *Polycyclic Aromatic Hydrocarbons/toxicity
MH  - *Receptors, Aryl Hydrocarbon/genetics/metabolism
PMC - PMC7327980
OTO - NOTNLM
OT  - Air pollution
OT  - Aryl hydrocarbon receptor
OT  - Inflammation
OT  - Oxidative stress
OT  - Particulate matter
OT  - Polycyclic aromatic hydrocarbons
COIS- Declaration of competing interest The authors declare that they have no competing 
      interests.
EDAT- 2020/05/02 06:00
MHDA- 2021/06/22 06:00
PMCR- 2020/04/18
CRDT- 2020/05/02 06:00
PHST- 2020/02/13 00:00 [received]
PHST- 2020/03/20 00:00 [revised]
PHST- 2020/03/31 00:00 [accepted]
PHST- 2020/05/02 06:00 [pubmed]
PHST- 2021/06/22 06:00 [medline]
PHST- 2020/05/02 06:00 [entrez]
PHST- 2020/04/18 00:00 [pmc-release]
AID - S2213-2317(20)30225-1 [pii]
AID - 101530 [pii]
AID - 10.1016/j.redox.2020.101530 [doi]
PST - ppublish
SO  - Redox Biol. 2020 Jul;34:101530. doi: 10.1016/j.redox.2020.101530. Epub 2020 Apr 
      18.