antioxidant/نخر

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Antioxidants and tumor necrosis factor alpha-inhibiting activity of sesame oil against doxorubicin-induced cardiotoxicity.

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OBJECTIVE Oxidative stress is currently considered to be the key factor in doxorubicin-induced cardiotoxicity. Comparatively small quantity of the endogenous antioxidant content of the heart is assumed to be the predisposing factor for doxorubicin-induced cardiotoxicity. The present research was

Effect of exogenous antioxidant enzymes and antioxidants on the development of endotoxin-induced hepatocellular necrosis in rats.

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To determine whether released oxidants in endotoxemia contribute to the development of hepatocellular necrosis, we examined the effects of antioxidants and antioxidant enzymes on endotoxin hepatotoxicity in rats. In rats given endotoxin, focal and random hepatocellular coagulative necrotic areas

Antioxidant potential of a novel tetrapeptide derivative in isoproterenol-induced myocardial necrosis in rats.

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A novel tetrapeptide derivative Boc-Lys(Boc)-Arg-Asp-Ser(tbu)-OtBu (PEP1261) has been tested in vivo in isoproterenol (ISO) hydrochloride (HCl)-induced myocardial necrosis in rats. ISO x HCl induces myocardial necrosis in rats which is accompanied by the distinct increase in heart weight, marked

Protection against pulmonary oxygen toxicity by interleukin-1 and tumor necrosis factor: role of antioxidant enzymes and effect of cyclooxygenase inhibitors.

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Rats injected with interleukin-1 (10 micrograms) and tumor necrosis factor (10 micrograms) and then exposed continuously to hyperoxia (greater than 99% O2, 1 atm) survived longer, had increased lung reduced/oxidized glutathione ratios, smaller pleural effusions, less pulmonary hypertension and

The apoptosis/necrosis transition in cerebellar granule cells depends on the mutual relationship of the antioxidant and the proteolytic systems which regulate ROS production and cytochrome c release en route to death.

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We investigate the death route induced by potassium depletion in cerebellar granule cells in 0-15 h time range and study whether and how mutual relationship occurs between the cell antioxidant and proteolytic system. To achieve this, we incubated cells in the absence or presence of inhibitors of the

Tumor necrosis factor-alpha in low doses preactivates and activates macrophages by increasing their ability to produce reactive oxygen species and oxidize low-density lipoproteins: protective effect of antioxidants.

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Tumor necrosis factor-alpha in low doses activated rat peritoneal macrophages and intensified production of reactive oxygen species (zymosan-depended chemiluminescence). Single or 2-fold incubation with tumor necrosis factor-a activated and preactivated human blood macrophages and promoted oxidative

Role of p55 tumor necrosis factor receptor 1 in acetaminophen-induced antioxidant defense.

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Tumor necrosis factor (TNF)-alpha is a macrophage-derived proinflammatory cytokine implicated in hepatotoxicity. In the present studies, p55 TNF receptor 1 (TNFR1) -/- mice were used to assess the role of TNF-alpha in acetaminophen-induced antioxidant defense. Treatment of wild-type (WT) mice with

Gene polymorphisms of tumor necrosis factor alpha and antioxidant enzymes in bronchial asthma.

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BACKGROUND Bronchial asthma is an inflammatory disease resulting from a combination of genetic and environmental factors. Single nucleotide polymorphisms in the regulatory regions of cytokine and antioxidant enzyme genes may affect cytokine production and enzyme activity, and thus play a

Activation of transcriptionally active nuclear factor-kappaB by tumor necrosis factor-alpha and its inhibition by antioxidants in rat thyroid FRTL-5 cells.

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ABSTRACT Tumor necrosis factor-alpha (TNF-alpha) exerts pleiotropic effects on thyroid follicular cells. However, the intracellular signaling pathway for the TNF-alpha action has not been well elucidated. The present study examined the effects of TNF-alpha on the activation of nuclear factor-kappa B

Resistance to tumor necrosis factor-alpha (TNF-alpha)-induced apoptosis in rat hepatoma cells expressing TNF-alpha is linked to low antioxidant enzyme expression.

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In order to study the mechanisms of resistance to tumor necrosis factor-alpha (TNF-alpha), we have constructed two stable transfectants producing TNF-alpha (Yv12-2 and Yv13-44) from the rat hepatoma H4IIE cell, which does not produce TNF-alpha. H4IIE cells were highly sensitive to apoptosis induced

Antioxidants attenuate nuclear factor-kappa B activation and tumor necrosis factor-alpha production in alcoholic hepatitis patient monocytes and rat Kupffer cells, in vitro.

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There is increased tumor necrosis factor-alpha (TNF) activity in alcoholic hepatitis (AH). OBJECTIVE To examine the effects of antioxidants and glutathione enhancing agents on NF-kappaB activation and TNF production in Kupffer cells and monocytes. METHODS Isolated rat Kupffer cells and peripheral

Inhibition of nuclear factor kappaB induces apoptosis following treatment with tumor necrosis factor alpha and an antioxidant in human prostate cancer cells.

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Transforming growth factor beta-1 (TGFbeta-1) and tumor necrosis factor alpha (TNF-alpha), an activator of nuclear factor kappa B (NF-kappaB), modulate apoptosis and/or cell growth. This study was designed to investigate the activity of NF-kappaB and its regulation of inhibitor of apoptosis gene

Mitochondria-targeted antioxidants do not prevent tumour necrosis factor-induced necrosis of L929 cells.

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Mitochondrial production of reactive oxygen species (ROS) is widely reported as a central effector during TNF-induced necrosis. The effect of a family of mitochondria-targeted antioxidants on TNF-induced necrosis of L929 cells was studied. While the commonly used lipid-soluble antioxidant BHA

[The effect of the antioxidant, butylhydroxyanisole on experimental myocardial necrosis in rats. Morphologic study].

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The present paper aimed to investigate a possible effect of the antioxidant butylhydroxyanisole (BHA) on the extent of experimental necroses of the myocardial cells. Administration of BHA in a daily dose of 10 mg.kg-1 i. m. lasted 20 days. The isoprenaline model in a single-dose subcutaneous

Antioxidants attenuate acute toxicity of tumor necrosis factor-alpha induced by brain injury in rat.

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Tumor necrosis factor-alpha alpha (TNF-alpha) and reactive oxygen species (ROS) are produced in the brain after traumatic injury and have deleterious effects. In a rat model of closed head injury (CHI), the synthetic antioxidant from the nitroxide family, Tempol, improved recovery and protected the

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