hydroxytoluene/necrosis

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Shifting necrosis: butylated hydroxytoluene (BHT) and phenobarbital move cocaine-induced hepatic necrosis across the lobule.

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Cocaine (60 mg/kg i.p.) caused centrilobular necrosis in the livers of 55% of DBA/2Ha mice. Pretreatment with phenobarbital (PB, 3 x 80 mg/kg i.p.) increased the incidence of necrosis to 70% and shifted this damage to the midzonal region. Pretreatment with butylated hydroxytoluene (BHT, 0.1% in

Effect of cobaltous chloride on butylated hydroxytoluene-induced hepatic necrosis in rats.

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Although a single dose of butylated hydroxytoluene (BHT); 1000 mg/kg to rats induced a hepatic injury accompanying centrilobular necrosis, the pretreatment with cobaltous chloride, an inhibitor of cytochrome P-450 synthesis, could inhibit the damage. The marked elevations of serum transaminase

Butylated hydroxytoluene and N-acetylcysteine attenuates tumor necrosis factor-alpha (TNF-alpha) secretion and TNF-alpha mRNA expression in alveolar macrophages from human lung transplant recipients in vitro.

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BACKGROUND Tumor necrosis factor-alpha (TNF-alpha) is a polypeptide cytokine principally produced by macrophages/monocytes and commonly associated with inflammatory conditions. The present study was designed to investigate whether the antioxidants butylated hydroxytoluene (BHT) and N-acetylcysteine

Protective effect of butylated hydroxytoluene on adriamycin-induced skin necrosis in the rat.

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The effect of butylated hydroxytoluene (BHT) on adriamycin (ADR)-induced skin ulcers was investigated using rats. The application of BHT reduced the size of the skin ulcers by the following amounts: topical application (20%); intradermal injection (50%); repeated applications of BHT (82%).

Amelioration of doxorubicin-induced skin necrosis in mice by butylated hydroxytoluene.

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The effect of butylated hydroxytoluene (BHT) on doxorubicin (Adriamycin)-induced skin ulcers was investigated in mice. The skin lesions produced by a single intradermal (ID) injection of doxorubicin (0.05 mg; 1 mg/ml) reached maximum size between 5 and 10 days after injection of ADR. Different

Lung injury induced by butylated hydroxytoluene: cytodynamic and biochemical studies in mice.

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Butylated hydroxytoluene, a common food additive, is known to produce proliferative pulmonary changes characterized by increased DNA, RNA, and lung weight. In the present study, reactive hyperplasia and fibrosis were produced within 9 days after a single intraperitoneal injection of 400 mg. per kg.

Reduced glutathione depletion causes necrosis and sensitization to tumor necrosis factor-alpha-induced apoptosis in cultured mouse hepatocytes.

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The effect of reduced glutathione (GSH) depletion by acetaminophen (APAP), diethylmaleate (DEM), or phorone on the mode of cell death and susceptibility to tumor necrosis factor (TNF)-induced cell death was studied in cultured mouse hepatocytes. Dose-dependent necrosis was the exclusive mode of cell

Enhancement of butylated hydroxytoluene-induced mouse lung damage by butylated hydroxyanisole.

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The phenolic antioxidant butylated hydroxytoluene (BHT) is known to produce a dose-dependent increase in mouse lung weight which is characterized by the necrosis of pulmonary type I and endothelial cells. We studied the ability of butylated hydroxyanisole (BHA) to modify BHT-induced changes in lung

On the mechanism of butylated hydroxytoluene-induced hepatic toxicity in rats.

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The relations between serum transaminase activity and the hepatic contents of glutathione and lipid peroxide were examined following oral administration to rats of butylated hydroxytoluene (BHT; 500 or 1000 mg/kg). The glutathione level rapidly diminished and reached a minimum at 6 hr after BHT

Antioxidants differentially regulate activation of nuclear factor-kappa B, activator protein-1, c-jun amino-terminal kinases, and apoptosis induced by tumor necrosis factor: evidence that JNK and NF-kappa B activation are not linked to apoptosis.

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Tumor necrosis factor (TNF) is known to mediate its signaling through generation of reactive oxygen species (ROS), but the type of TNF signal regulated by ROS and the nature of the ROS species involved are not fully understood. In this report, we investigated the effect of various superoxide radical

Butylated hydroxyanisole inhibits tumor necrosis factor-induced cytotoxicity and arachidonic acid release.

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The mechanisms by which the antioxidant butylated hydroxyanisole (BHA) inhibits recombinant tumor necrosis factor alpha (rTNF-alpha)-induced cytotoxicity have been studied in WEHI 164 clone 13 (WEHI) and L929 fibrosarcoma cells. When BHA was added simultaneously with rTNF-alpha, it completely

The site specificity and sensitivity of the rat liver to butylated hydroxytoluene-induced damage.

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The food additive butylated hydroxytoluene (BHT) is capable of damaging centrilobular or periportal cells in the liver according to the dose and duration of treatment. The effect of two hepatotoxicity potentiating agents on the site specificity of acute cell damage was investigated in Sprague-Dawley

Butylated hydroxyanisole specifically inhibits tumor necrosis factor-induced cytotoxicity and growth enhancement.

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The effect of commonly used food antioxidants on recombinant tumor necrosis factor alpha (rTNF-alpha)-induced cytotoxicity, growth enhancement and adhesion has been evaluated. Butylated hydroxyanisole (BHA) and 4-hydroxymethyl-2,6-di-t-butylphenol (HBP) were the only two of nine antioxidants that

Nephrotoxicity of butylated hydroxytoluene in phenobarbital-pretreated male rats.

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A single large dose of butylated hydroxytoluene (BHT, 1000 mg/kg) in male Fischer 344 rats produced some renal damage, reduced accumulation of p-aminohippuric acid in renal slices, proteinuria and enzymuria, in addition to hepatic damage. Further, prior administration of phenobarbital (80 mg/kg,

Pneumotoxicity of butylated hydroxytoluene applied dermally to CD-1 mice.

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Pneumotoxicity of butylated hydroxytoluene (BHT) applied to the skin of CD-1 mice was investigated and compared with that of butylated hydroxyanisole (BHA). To 6 groups of 10 male mice and 10 female mice 0.1 ml of dimethylsulfoxide (DMSO) solutions containing 0, 5, 10, 20, or 30 mg of BHT or 30 mg

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