flavin-mononucleotide and Necrosis

flavin-mononucleotide has been researched along with Necrosis* in 2 studies

Other Studies

2 other study(ies) available for flavin-mononucleotide and Necrosis

ArticleYear
[Pharmacological neuroprotection against brain damage in ischemiai/reperfusion experiment].
    Eksperimental'naia i klinicheskaia farmakologiia, 2011, Volume: 74, Issue:8

    Experiment carried out on laboratory animals (rats) were aimed at comparative evaluation of the effect of several neuroprotective drugs under the conditions of model brain ischemia-reperfusion. The experimental methods included staining of brain tissue sections by hematoxiline-eosine, Nissl staining, and expression of NOS1, NOS3, TRAIL by imunnohistological means. The intensity of damage in various parts of brain and the nature of apoptosis without neuroprotection and with popular neuroprotectors (cytoflavin, actovegin, mexidol) and a test drug at the stage ofpreclinical trial (AKF-90-7) were evaluated. Characteristic cytotoxic (coagulative pycnomorphic and colliquative necrosis of neurons) and vascular (hemostasia, erythropedesis) changes were revealed. The neuroprotective effectof drugs decreases in the following order: AKF-90-7 > cytoflavin > actovegin > mexidol.

    Topics: Animals; Brain; Drug Combinations; Drug Evaluation, Preclinical; Eosine Yellowish-(YS); Flavin Mononucleotide; Glycine; Hematoxylin; Heme; Hemostasis; Immunohistochemistry; Inosine Diphosphate; Male; Necrosis; Neurons; Neuroprotective Agents; Niacinamide; Nitric Oxide Synthase Type I; Nitric Oxide Synthase Type III; Picolines; Rats; Rats, Inbred Strains; Reperfusion Injury; Succinates; TNF-Related Apoptosis-Inducing Ligand

2011
Role of mammalian cytosolic molybdenum Fe-S flavin hydroxylases in hepatic injury.
    Life sciences, 2008, Mar-26, Volume: 82, Issue:13-14

    The study was designed to investigate the role of molybdenum iron-sulfur flavin hydroxylases in the pathogenesis of liver injuries induced by structurally and mechanistically diverse hepatotoxicants. While carbon tetrachloride (CCl4), thioacetamide (TAA) and chloroform (CHCl3) inflict liver damage by producing free radicals, acetaminophen (AAP) and bromobenzene (BB) exert their effects by severe glutathione depletion. Appropriate doses of these compounds were administered to induce liver injury in rats. The activities of the Mo-Fe-S flavin hydroxylases were measured and correlated with the biochemical markers of hepatic injury. The activity levels of the anti-oxidative enzymes and glutathione redox cycling enzymes were also determined. The treatment of rats with the hepatotoxins that inflict liver injury by generating free radicals (CCl4, TAA, CHCl3) had elevated activity levels of hepatic Mo-Fe-S flavin hydroxylases (p<0.05). Specific inhibition of these hydroxylases by their common inhibitor, sodium tungstate, suppresses biochemical and oxidative stress markers of hepatic tissue damage. On the contrary, Mo-Fe-S flavin hydroxylases did not show any change in animals receiving AAP and BB. Correspondingly, sodium tungstate could not attenuate damage in AAP and BB treated groups of rats. The study concludes that Mo-Fe-S hydroxylases contribute to the hepatic injury inflicted by free radical generating agents and does not play any role in hepatic injury produced by glutathione depleting agents. The study has implication in understanding human liver diseases caused by a variety of agents, and to investigate the efficacy of the inhibitors of Mo-Fe-S flavin hydroxylases as potential therapeutic agents.

    Topics: Aldehyde Oxidase; Animals; Antioxidants; Chemical and Drug Induced Liver Injury; Coenzymes; Cytosol; Female; Flavin Mononucleotide; Liver; Metalloproteins; Molybdenum Cofactors; Necrosis; Oxidative Stress; Pteridines; Rats; Rats, Wistar; Xanthine Oxidase

2008
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