Early steps in bilirubin-mediated apoptosis in murine hepatoma (Hepa 1c1c7) cells are characterized by aryl hydrocarbon receptor-independent oxidative stress and activation of the mitochondrial pathway

2005 ◽  
Vol 19 (4) ◽  
pp. 244-255 ◽  
Author(s):  
Garth H. Oakes ◽  
John R. Bend
Keyword(s):  
Oxidative Stress ◽  
Aryl Hydrocarbon Receptor ◽  
Mitochondrial Pathway ◽  
Aryl Hydrocarbon

Exposure of human skin to benzo[a]pyrene: Role of CYP1A1 and aryl hydrocarbon receptor in oxidative stress generation

Toxicology ◽  
2010 ◽  
Vol 271 (3) ◽  
pp. 83-86 ◽  
Author(s):  
C. Costa ◽  
S. Catania ◽  
R. De Pasquale ◽  
R. Stancanelli ◽  
G.M. Scribano ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Aryl Hydrocarbon Receptor ◽  
Human Skin ◽  
Stress Generation ◽  
Aryl Hydrocarbon

scholarly journals Induction of Oxidative Stress Responses by Dioxin and other Ligands of the Aryl Hydrocarbon Receptor

Dose-Response ◽  
2005 ◽  
Vol 3 (3) ◽  
pp. dose-response.0 ◽  
Author(s):  
John F. Reichard ◽  
Timothy P. Dalton ◽  
Howard G. Shertzer ◽  
Alvaro Puga
Keyword(s):  
Oxidative Stress ◽  
Aryl Hydrocarbon Receptor ◽  
Stress Responses ◽  
Species Difference ◽  
Large Species ◽  
Vitro Assay ◽  
Oxygen Generation ◽  
Aryl Hydrocarbon ◽  
Dioxin Exposure

TCDD and other polyhalogenated aromatic hydrocarbon ligands of the aryl hydrocarbon receptor (AHR) have been classically considered as non-genotoxic compounds because they fail to be directly mutagenic in either bacteria or most in vitro assay systems. They do so in spite of having repeatedly been linked to oxidative stress and to mutagenic and carcinogenic outcomes. Oxidative stress, on the other hand, has been used as a marker for the toxicity of dioxin and its congeners. We have focused this review on the connection between oxidative stress induction and the toxic effects of fetal and adult dioxin exposure, with emphasis on the large species difference in sensitivity to this agent. We examine the roles that the dioxin-inducible cytochromes P450s play in the cellular and toxicological consequences of dioxin exposure with emphasis on oxidative stress involvement. Many components of the health consequences resulting from dioxin exposure may be attributable to epigenetic mechanisms arising from prolonged reactive oxygen generation.

scholarly journals Involvement of the Microglial Aryl Hydrocarbon Receptor in Neuroinflammation and Vasogenic Edema after Ischemic Stroke

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 718
Author(s):  
Miki Tanaka ◽  
Masaho Fujikawa ◽  
Ami Oguro ◽  
Kouichi Itoh ◽  
Christoph F. A. Vogel ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ischemic Stroke ◽  
Aryl Hydrocarbon Receptor ◽  
Vasogenic Edema ◽  
Artery Occlusion ◽  
Aryl Hydrocarbon ◽  
Inflammatory Conditions ◽  
Severity Scores ◽  
Factor Α ◽  
Cerebral Artery Occlusion

Microglia are activated after ischemic stroke and induce neuroinflammation. The expression of the aryl hydrocarbon receptor (AhR) has recently been reported to elicit cytokine expression. We previously reported that microglial activation mediates ischemic edema progression. Thus, the purpose of this study was to examine the role of AhR in inflammation and edema after ischemia using a mouse middle cerebral artery occlusion (MCAO) model. MCAO upregulated AhR expression in microglia during ischemia. MCAO increased the expression of tumor necrosis factor α (TNFα) and then induced edema progression, and worsened the modified neurological severity scores, with these being suppressed by administration of an AhR antagonist, CH223191. In THP-1 macrophages, the NADPH oxidase (NOX) subunit p47phox was significantly increased by AhR ligands, especially under inflammatory conditions. Suppression of NOX activity by apocynin or elimination of superoxide by superoxide dismutase decreased TNFα expression, which was induced by the AhR ligand. AhR ligands also elicited p47phox expression in mouse primary microglia. Thus, p47phox may be important in oxidative stress and subsequent inflammation. In MCAO model mice, P47phox expression was upregulated in microglia by ischemia. Lipid peroxidation induced by MCAO was suppressed by CH223191. Taken together, these findings suggest that AhR in the microglia is involved in neuroinflammation and subsequent edema, after MCAO via p47phox expression upregulation and oxidative stress.

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