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Tumor necrosis factor-α inhibits effects of aryl hydrocarbon receptor ligands on cell death in human lymphocytes.

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BACKGROUND Activation of aryl hydrocarbon receptor (AhR) leads to diverse outcome in various kinds of cells. AhR activation may induce apoptosis or prevent of apoptosis and cell death. Recent studies suggest that apoptosis effects of AhR can be modulated by inflammatory cytokine like tumor necrosis

Acute exposure to aliphatic hydrocarbons: an unusual cause of acute tubular necrosis.

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Acute tubular necrosis is not an uncommon phenomenon, but it rarely results from environmental factors. We describe a patient in whom acute renal failure developed 2 times after overexposure to aliphatic hydrocarbons and discuss some potential pathophysiological mechanisms. This association has

Down-regulation of aryl hydrocarbon receptor-regulated genes by tumor necrosis factor-alpha and lipopolysaccharide in murine hepatoma Hepa 1c1c7 cells.

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Although much is known concerning the effects of inflammation and oxidative stress on the cytochrome P450 1A1 (CYP1A1), little is known about the modulation of other aryl hydrocarbon receptor (AHR)-regulated genes such as glutathione-S-transferase Ya (GST Ya) and NAD(P)H:quinone oxidoreductase (QOR)

Aryl hydrocarbon receptor modulation of tumor necrosis factor-alpha-induced apoptosis and lysosomal disruption in a hepatoma model that is caspase-8-independent.

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Recent studies suggest that the aryl hydrocarbon receptor (AhR) modulates susceptibilities to some pro-apoptotic agents. AhR-containing murine hepatoma 1c1c7 cultures underwent apoptosis following exposure to tumor necrosis factor-alpha (TNFalpha) + cycloheximide (CHX). In contrast, Tao cells, an

Protective action of polycyclic hydrocarbons against induction of adrenal necrosis by dimethylbenzanthracene.

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Treatment of rats with certain polycyclic hydrocarbons shifts the hydroxylation of dimethylbenzanthracene (DMBA) by liver microsomes from the side-chain to the ring. Protection by these hydrocarbons against dimethylbenzanthracene-induced adrenal necrosis is possibly achieved by decreasing the yield

Endogenous aryl hydrocarbon receptor promotes basal and inducible expression of tumor necrosis factor target genes in MCF-7 cancer cells.

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The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that upon activation by the toxicant 2,3,7,8 tetrachlorodibenzo-p-dioxin (TCDD) stimulates gene expression and toxicity. AHR is also important for normal mouse physiology and may play a role in cancer progression in the

Tumor necrosis factor-alpha modulates effects of aryl hydrocarbon receptor ligands on cell proliferation and expression of cytochrome P450 enzymes in rat liver "stem-like" cells.

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Various liver diseases lead to an extensive inflammatory response and release of a number of proinflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha). This cytokine is known to play a major role in liver regeneration as well as in carcinogenesis. We investigated possible

Crosstalk between tumor necrosis factor-alpha signaling and aryl hydrocarbon receptor signaling in nuclear factor -kappa B activation: A possible molecular mechanism underlying the reduced efficacy of TNF-inhibitors in rheumatoid arthritis by smoking.

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To examine the influence of smoking on biologics treatment against different therapeutic targets, such as TNFα, IL-6, and T cell, in rheumatoid arthritis (RA) and elucidate the underlying molecular mechanism.The association between drug-discontinuation due

INHIBITORY EFFECT OF POLYNUCLEAR HYDROCARBONS AND AMPHENONE ANALOGS ON INDUCTION OF ACUTE ADRENAL NECROSIS BY 7,12-DIMETHYLBENZ(ALPHA)ANTHRACENE.

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[Halogenated hydrocarbon compounds in anesthesia and their effect on the liver. Liver necrosis and tubulus degeneration after repeated methoxyflurane anesthesia].

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Suppression of 7,12-dimethylbenz( )anthracene-produced adrenal necrosis by steroids capable of inducing aryl hydrocarbon hydroxylase.

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hydrocarbon/nekros

Tumor necrosis factor-α inhibits effects of aryl hydrocarbon receptor ligands on cell death in human lymphocytes.

Acute exposure to aliphatic hydrocarbons: an unusual cause of acute tubular necrosis.

Down-regulation of aryl hydrocarbon receptor-regulated genes by tumor necrosis factor-alpha and lipopolysaccharide in murine hepatoma Hepa 1c1c7 cells.

Aryl hydrocarbon receptor modulation of tumor necrosis factor-alpha-induced apoptosis and lysosomal disruption in a hepatoma model that is caspase-8-independent.

Protective action of polycyclic hydrocarbons against induction of adrenal necrosis by dimethylbenzanthracene.

Endogenous aryl hydrocarbon receptor promotes basal and inducible expression of tumor necrosis factor target genes in MCF-7 cancer cells.

Tumor necrosis factor-alpha modulates effects of aryl hydrocarbon receptor ligands on cell proliferation and expression of cytochrome P450 enzymes in rat liver "stem-like" cells.

Crosstalk between tumor necrosis factor-alpha signaling and aryl hydrocarbon receptor signaling in nuclear factor -kappa B activation: A possible molecular mechanism underlying the reduced efficacy of TNF-inhibitors in rheumatoid arthritis by smoking.

INHIBITORY EFFECT OF POLYNUCLEAR HYDROCARBONS AND AMPHENONE ANALOGS ON INDUCTION OF ACUTE ADRENAL NECROSIS BY 7,12-DIMETHYLBENZ(ALPHA)ANTHRACENE.

[Halogenated hydrocarbon compounds in anesthesia and their effect on the liver. Liver necrosis and tubulus degeneration after repeated methoxyflurane anesthesia].

Suppression of 7,12-dimethylbenz( )anthracene-produced adrenal necrosis by steroids capable of inducing aryl hydrocarbon hydroxylase.

SOME CONSIDERATIONS ON MOLECULAR STRUCTURES OF POLYNUCLEAR HYDROCARBONS AND INHIBITION OF ADRENAL NECROSIS IN RATS.

Centrolobular hepatic necrosis related to covalent binding of metabolites of halogenated aromatic hydrocarbons.

Metabolism and binding of aromatic hydrocarbons in the lung. Relationship to experimental bronchiolar necrosis.

Biochemical mechanism of hepatic necrosis induced by aromatic hydrocarbons.

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