يعرض 1 - 3 نتائج من 3 نتيجة بحث عن '"Lactate dehydrogenase"', وقت الاستعلام: 0.81s تنقيح النتائج
  1. 1

    المصدر: Brazilian Journal of Medical and Biological Research v.40 n.6 2007
    Brazilian Journal of Medical and Biological Research
    Associação Brasileira de Divulgação Científica (ABDC)
    instacron:ABDC
    Brazilian Journal of Medical and Biological Research, Volume: 40, Issue: 6, Pages: 857-865, Published: JUN 2007
    Brazilian Journal of Medical and Biological Research, Vol 40, Iss 6, Pp 857-865 (2007)

    الوصف: We investigated whether hepatic artery endothelium may be the earliest site of injury consequent to liver ischemia and reperfusion. Twenty-four heartworm-free mongrel dogs of either sex exposed to liver ischemia/reperfusion in vivo were randomized into four experimental groups (N = 6): a) control, sham-operated dogs, b) dogs subjected to 60 min of ischemia, c) dogs subjected to 30 min of ischemia and 60 min of reperfusion, and d) animals subjected to 45 min of ischemia and 120 min of reperfusion. The nitric oxide endothelium-dependent relaxation of hepatic artery rings contracted with prostaglandin F2a and exposed to increasing concentrations of acetylcholine, calcium ionophore A23187, sodium fluoride, phospholipase-C, poly-L-arginine, isoproterenol, and sodium nitroprusside was evaluated in organ-chamber experiments. Lipid peroxidation was estimated by malondialdehyde activity in liver tissue samples and by blood lactic dehydrogenase (LDH), serum aspartate aminotransferase (AST) and serum alanine aminotransferase (ALT) activities. No changes were observed in hepatic artery relaxation for any agonist tested. The group subjected to 45 min of ischemia and 120 min of reperfusion presented marked increases of serum aminotransferases (ALT = 2989 ± 1056 U/L and AST = 1268 ± 371 U/L; P < 0.01), LDH = 2887 ± 1213 IU/L; P < 0.01) and malondialdehyde in liver samples (0.360 ± 0.020 nmol/mgPT; P < 0.05). Under the experimental conditions utilized, no abnormal changes in hepatic arterial vasoreactivity were observed: endothelium-dependent and independent hepatic artery vasodilation were not impaired in this canine model of ischemia/reperfusion injury. In contrast to other vital organs and in the ischemia/reperfusion injury environment, dysfunction of the main artery endothelium is not the first site of reperfusion injury.

    وصف الملف: text/html

  2. 2

    المساهمون: Universidade Federal de São Paulo (UNIFESP)

    المصدر: Repositório Institucional da UNIFESP
    Universidade Federal de São Paulo (UNIFESP)
    instacron:UNIFESP
    Brazilian Journal of Medical and Biological Research, Vol 40, Iss 3, Pp 343-348 (2007)
    Brazilian Journal of Medical and Biological Research v.40 n.3 2007
    Brazilian Journal of Medical and Biological Research
    Associação Brasileira de Divulgação Científica (ABDC)
    instacron:ABDC
    Brazilian Journal of Medical and Biological Research, Volume: 40, Issue: 3, Pages: 343-348, Published: MAR 2007

    الوصف: Animal studies and premarketing clinical trials have revealed hepatotoxicity of statins, primarily minor elevations in serum alanine aminotransferase levels. The combined chronic use of medicines and eventual ethanol abuse are common and may present a synergistic action regarding liver injury. Our objective was to study the effect of the chronic use of atorvastatin associated with acute ethanol administration on the liver in a rat model. One group of rats was treated daily for 5 days a week for 2 months with 0.8 mg/kg atorvastatin by gavage. At the end of the treatment the livers were perfused with 72 mM ethanol for 60 min. Control groups (at least 4 animals in each group) consisted of a group of 2-month-old male Wistar EPM-1 rats exposed to 10% ethanol (v/v) ad libitum replacing water for 2 months, followed by perfusion of the liver with 61 nM atorvastatin for 60 min, and a group of animals without chronic ethanol treatment whose livers were perfused with atorvastatin and/or ethanol. The combination of atorvastatin with ethanol did not increase the release of injury marker enzymes (alanine aminotransferase, aspartate aminotransferase, and lactic dehydrogenase) from the liver and no change in liver function markers (bromosulfophthalein clearance, and oxygen consumption) was observed. Our results suggest that the combination of atorvastatin with ethanol is not more hepatotoxic than the separate use of each substance. Universidade Federal de São Paulo (UNIFESP) Escola Paulista de Medicina Departamento de Bioquímica Universidade Federal de São Paulo (UNIFESP) Escola Paulista de Medicina Departamento de Medicina UNIFESP, EPM, Depto. de Bioquímica UNIFESP, EPM, Depto. de Medicina SciELO

    وصف الملف: text/html

  3. 3

    المصدر: Brazilian Journal of Medical and Biological Research, Volume: 34, Issue: 8, Pages: 1055-1064, Published: AUG 2001
    Scopus-Elsevier
    Brazilian Journal of Medical and Biological Research, Vol 34, Iss 8, Pp 1055-1064 (2001)
    Brazilian Journal of Medical and Biological Research v.34 n.8 2001
    Brazilian Journal of Medical and Biological Research
    Associação Brasileira de Divulgação Científica (ABDC)
    instacron:ABDC

    الوصف: The effects of short-term burst (5 min at 1.8 m/s) swimming and long-term cruiser (60 min at 1.2 m/s) swimming on maximal enzyme activities and enzyme distribution between free and bound states were assessed for nine glycolytic and associated enzymes in tissues of horse mackerel, Trachurus mediterraneus ponticus. The effects of exercise were greatest in white muscle. The activities of phosphofructokinase (PFK), pyruvate kinase (PK), fructose-1,6-bisphosphatase (FBPase), and phosphoglucomutase (PGM) all decreased to 47, 37, 37 and 67%, respectively, during 60-min exercise and all enzymes except phosphoglucoisomerase (PGI) and PGM showed a change in the extent of binding to subcellular particulate fractions during exercise. In red muscle, exercise affected the activities of PGI, FBPase, PFK, and lactate dehydrogenase (LDH) and altered percent binding of only PK and LDH. In liver, exercise increased the PK activity 2.3-fold and reduced PGI 1.7-fold only after 5 min of exercise but altered the percent binding of seven enzymes. Fewer effects were seen in brain, with changes in the activities of aldolase and PGM and in percent binding of hexokinase, PFK and PK. Changes in enzyme activities and in binding interactions with subcellular particulate matter appear to support the altered demands of tissue energy metabolism during exercise.

    وصف الملف: text/html