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Journal ArticleDOI

N-acetylcysteine and glutathione as inhibitors of tumor necrosis factor production.

TLDR
The results indicated that oral administration of NAC protects against LPS toxicity and inhibits the increase in serum TNF levels in LPS-treated mice, and data indicate that GSH can be an endogenous modulator of TNF production in vivo.
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This article is published in Cellular Immunology.The article was published on 1992-04-01. It has received 234 citations till now. The article focuses on the topics: Tumor necrosis factor production & Glutathione.

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Citations
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Journal ArticleDOI

Oxidative stress and regulation of glutathione in lung inflammation

TL;DR: The redox control and involvement of nuclear factor-kappaB and activator protein-1 in the regulation of cellular glutathione and gamma-glutamylcysteine synthetase under conditions of oxidative stress and inflammation are described.
Journal ArticleDOI

Pharmacological actions of melatonin in oxygen radical pathophysiology

TL;DR: Whether the quantity of melatonin produced in vertebrate species is sufficient to significantly influence the total antioxidative defense capacity of the organism remains unknown, but its pharmacological benefits seem assured considering the low toxicity of the molecule.
Journal ArticleDOI

Regulation of redox glutathione levels and gene transcription in lung inflammation: therapeutic approaches

TL;DR: The role of GSH levels in the regulation of transcription factors, whose activation and DNA binding leads to proinflammatory and antioxidant gene transcription is featured and the potential role of thiol antioxidants as a therapeutic approach in inflammatory lung diseases is discussed.
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Cytokine production by human airway epithelial cells after exposure to an air pollution particle is metal-dependent

TL;DR: It is demonstrated that metals present in ROFA may be responsible for production and release of inflammatory mediators by the respiratory tract epithelium and suggested that these mediators may contribute to the toxic effects of particulate air pollutants reported in epidemiology studies.
Journal ArticleDOI

Role of oxidants/antioxidants in smoking-induced lung diseases

TL;DR: The evidence for the presence of an oxidant/antioxidant imbalance in smoking-induced lung disease and its relevance to therapy in these conditions is reviewed.
References
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Journal ArticleDOI

Estimation of total, protein-bound, and nonprotein sulfhydryl groups in tissue with Ellman's reagent

TL;DR: A simple spectrophotometric method for the routine concomitant determination of sulfhydryl groups in PB- SH, NP-SH, and T-SH fractions in various tissues is reported.
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Oxygen-derived free radicals in postischemic tissue injury.

TL;DR: It is now clear that oxygen-derived free radicals play an important part in several models of experimentally induced reperfusion injury, and Dysfunction induced by free radicals may be a major component of ischemic diseases of the heart, bowel, liver, kidney, and brain.
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Anti-cachectin/TNF monoclonal antibodies prevent septic shock during lethal bacteraemia

TL;DR: Protection against shock, vital organ dysfunction, persistent stress hormone release and death was conferred by administration of antibodies 2 h before bacterial infusion, indicating that cachectin is a mediator of fatal bacteraemic shock and suggesting that antibodies against Cachectin offer a potential therapy of life-threatening infection.
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Passive immunization against cachectin/tumor necrosis factor protects mice from lethal effect of endotoxin

TL;DR: The data suggest that cachectin/TNF is one of the principal mediators of the lethal effect of endotoxin, and this effect was dose-dependent and was most effective when the antiserum was administered prior to the injection of the endotoxin.
Journal ArticleDOI

The antioxidant action of N-acetylcysteine: its reaction with hydrogen peroxide, hydroxyl radical, superoxide, and hypochlorous acid.

TL;DR: N-acetylcysteine is a powerful scavenger of hypochlorous acid (H--OCl); low concentrations are able to protect alpha 1-antiproteinase against inactivation by HOCl.
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