Relevance of the Aryl Hydrocarbon Receptor (AhR) for Clinical Toxicology
Abstract
INTRODUCTION: The aryl hydrocarbon receptor (AhR) is a cellular signaling molecule infamous for mediating the toxicity of dioxins and related compounds. AIM: The aim of this review is to provide a background of AhR and to examine critically its role in chemical toxicity, in physiological systems, and its interaction with drugs and other compounds. TOXICITY: The AhR is essential for the toxicity of dioxins and related chemicals. The AhR mediates the exquisite sensitivity of animals to dioxins, where as little as 2 ng/kg/day can yield striking adverse effects. PHYSIOLOGICAL ROLE OF AHR: The wide variety of adverse effects of dioxin argues for an important role of the AhR in a variety of physiological systems. Recent investigations have highlighted the role of AhR in the development of the brain and vasculature. DRUGS AND OTHER CHEMICAL ACTIVATORS OF AHR: The development of AhR agonists during drug development programs is sometimes inadvertent, but sometimes the target of development, and is yet further confirmation of the likely importance of AhR signaling in constitutive physiology. The presence of AhR agonists in the diet such as indolo-(3,2-b)-carbazole and 3,3'-diindolylmethane (metabolized from indole 3-carbinol), flavonoids, and sulforaphane and of endogenous activators of this signaling system such as eicosanoids, indirubin, bilirubin, cAMP, and tryptophan are suggestive that AhR activation is a normal physiological process and that it is the persistent and high-level stimulation of AhR by dioxins that is responsible for toxicity. CONCLUSIONS: AhR-mediated toxicity and physiology are highly relevant to clinical toxicology and drug development.
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TEFs have been used to characterize the toxicity of polychlorinated chemicals because their mechanism of toxicity appears to result from activation of a specific receptor.
“For example, TEFs have been used to characterize the toxicity of polychlorinated chemicals because their mechanism of toxicity appears to result from the activation of a specific receptor [47].”
From The EU’s Per- and Polyfluoroalkyl Substances (PFAS) Ban: A Case of Policy over Science (2023) · cites this paper as [47]
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Recombinant expression of aryl hydrocarbon receptor for quantitative ligand-binding analysis
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“The aryl hydrocarbon receptor (AHR) is a central paradigm of modern toxicology (Bradshaw and Bell 2009; Zhou 2016).”
Background
- Authors
- Bradshaw, T. D., & Bell, D. R.
- Affiliations
- University of Nottingham (GB)
- Corresponding author
- Bell, David R.
- Venue
- Clinical Toxicology
- Publisher
- Informa UK Limited
- Published
- 2009-07-30
- Volume
- 47
- Issue
- 7
- Pages
- 632-642
- ISSN
- 0009-9309 (ISSN-L)
- 1556-3650
- 1556-9519
- OpenAlex
- W2048025515
- Cited by
- 62
- References
- 121
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 2 · 2023: 5 · 2022: 2 · 2021: 3 · 2020: 2 · 2019: 6 · 2018: 5 · 2017: 4 · 2016: 1 · 2015: 2 · 2014: 6 · 2013: 1 · 2012: 8
- FWCI
- 0.81
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Clinical Toxicology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Toxic Organic Pollutants Impact
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Pharmacogenetics and Drug Metabolism
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
- Keywords
- aryl hydrocarbon receptor, dioxins, AhR agonists, drug-drug interactions, indole-3-carbinol, 3,3'-diindolylmethane, flavonoids, sulforaphane, eicosanoids, tryptophan, brain development, vascular development, chemical toxicity
- MeSH terms
- Animals, Dioxins, Drug Interactions, Humans, Toxicology, Receptors, Aryl Hydrocarbon, Drug Discovery
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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