alcohol dehydrogenase/necrosis

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Polymorphism of tumor necrosis factor-beta and alcohol dehydrogenase genes and alcoholic brain atrophy in Japanese patients.

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BACKGROUND Alcohol abuse can induce brain atrophy, but it only occurs in some alcoholics. Many inflammatory cytokines such as tumor necrosis factor (TNF) are produced rapidly in the brain by experimental or clinical injury. METHODS To investigate whether genetic polymorphism of TNF was related to

Liver cell necrosis in rats after prolonged ethanol ingestion under the influence of an alcohol-dehydrogenase inhibitor.

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[Glutamic dehydrogenase and alcohol dehydrogenase of blood in various conditions of experimental hepatic necrosis: hepatitis due to MHV-3 virus, acute poisoning due to carbon tetrachloride].

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Coding and non-coding polymorphisms in alcohol dehydrogenase alters protein expression and alcohol-associated erythema.

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Ethanol (EtOH), isopropyl alcohol (IPA), and propylene glycol (PG) increase topical drug delivery, but are sometimes associated with erythema. A potential genetic basis for alcohol-associated erythema was investigated as the function of polymorphisms in coding and non-coding regions of class IB

Murine pro-tumor necrosis factor expressed in Saccharomyces cerevisiae HF7c localizes to membrane/particulate.

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Tumor necrosis factor (TNF) is a cytokine that is produced by immune cells in response to bacterial and viral stimuli and plays important roles in various inflammatory diseases. TNF is produced as a membrane-bound precursor, which is then cleaved to release soluble mature protein. We expressed

Pre-existing liver cirrhosis reduced the toxic effect of diethylene glycol in a rat model due to the impaired hepatic alcohol dehydrogenase.

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Hepatic metabolizing enzymes of diethylene glycol (DEG) are impaired in liver diseases. Thus, the purpose of this study was to increase our understandings in metabolism and toxicology of DEG by clarifying the influences of pre-existing liver disease. Forty Sprague-Dawley rats with carbon

Hepatotoxicity due to allyl alcohol in deermice depends on alcohol dehydrogenase.

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The role of alcohol dehydrogenase in the hepatic necrosis due to allyl alcohol was studied in two strains of the deermouse, Peromyscus maniculatus. Mice of the alcohol dehydrogenase-negative (AdhN) strain which lack alcohol dehydrogenase activity were resistant to allyl alcohol toxicity. In

Alcohol dehydrogenase: a new sensitive marker of hepatic centrilobular damage.

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To determine whether serum alcohol dehydrogenase (ADH) activity reflects hepatic damage of centrilobular region (zone 3), the rats were given either bromobenzene (BB) or allyl alcohol (AA) IP to produce the pericen tral or periportal necrosis respectively. After AA or BB serum alanine

Hyaluronidase induction of a WW domain-containing oxidoreductase that enhances tumor necrosis factor cytotoxicity.

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To determine how hyaluronidase increases certain cancer cell sensitivity to tumor necrosis factor (TNF) cytotoxicity, we report here the isolation and characterization of a hyaluronidase-induced murine WW domain-containing oxidoreductase (WOX1). WOX1 is composed of two N-terminal WW domains, a

[Chemistry and biological effects of gliotoxin].

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Gliotoxin is a mycotoxin from the epipolythiodioxypipeazine family with biological active internal disulfide bridge. Gliotoxin has an antibacterial and antiviral activity, but it was discarded from clinical practice due to its toxicity. The most studied effect of gliotoxin is its influence on the

Evidence for variation in the optimal translation initiation complex: plant eIF4B, eIF4F, and eIF(iso)4F differentially promote translation of mRNAs.

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Eukaryotic initiation factor (eIF) 4B is known to interact with multiple initiation factors, mRNA, rRNA, and poly(A) binding protein (PABP). To gain a better understanding of the function of eIF4B, the two isoforms from Arabidopsis (Arabidopsis thaliana) were expressed and analyzed using biophysical

Hypermetabolic state and hypoxic liver damage.

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The concept of a hypermetabolic state to explain metabolic tolerance to ethanol grew from the recognition that the rate of alcohol metabolism is, in general, limited by the rate at which mitochondria can reoxidize reducing equivalents and thus by the rate at which oxygen can be consumed by the

Effect of verapamil on allyl alcohol hepatotoxicity.

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The effects of verapamil, a calcium channel blocker, on allyl alcohol (AA) hepatotoxicity were studied in vivo. AA administration induced an increase of serum alanine aminotransferase (ALT) concentration and liver necrosis by means of glutathione (GSH) depletion. Pretreatment with verapamil reduced

On the nature of the 'nothing dehydrogenase' reaction.

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The biochemical mechanism underlying the 'nothing dehydrogenase' reaction during the histochemical demonstration of dehydrogenases using tetranitro BT as the final electron acceptor has been investigated in unfixed, frozen rat liver sections. The reaction is stronger with NAD+ than either with NADP+

High dosing of α-tocopherol inhibits rat liver regeneration by modifying signal transducer and activator of transcription protein expression and its correlation with cell redox state and retinoid metabolism.

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Lipid peroxidation (LP) promoted by partial hepatectomy (PH) is qualitatively distinct among subcellular fractions and temporally transient, probably being a necessary physiological event for rat liver regeneration. In fact, α-tocopherol (vitamin E [VE]) exerts adverse effects, partially inhibiting

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