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  • 1995-1999  (3)
  • 1
    ISSN: 1573-2568
    Keywords: CHRONIC HEPATITIS ; HEPATITIS B VIRUS INFECTION ; HEPATITIS C VIRUS INFECTION ; AMYLASE ; LIPASE
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Serum amylase and lipase concentrations weredetermined in 78 patients with chronic liver diseases[26 chronic active hepatitis (CAH) and 52 livercirrhosis] and in 15 healthy subjects. Pancreaticisoamylase concentrations and macroamylase complexes wereassayed in hyperamylasemic sera. Serum amylase levelswere abnormally elevated in 27 patients (35%; 22 livercirrhosis, 5 CAH), whereas serum lipase levels were elevated in 16 patients (21%; 15 livercirrhosis, 1 CAH). In 9 of the 27 hyperamylasemicpatients, the hyperamylasemia was of pancreatic type.Macroamylasemic complexes were not detected inhyperamylasemic sera. Patients with liver cirrhosis had serumlevels of amylase and lipase significantly higher thanboth the healthy subjects and the patients with CAH,while no significant differences were found in serum levels of these enzymes in patients with CAH ascompared to the healthy subjects. A decreased livermetabolism of serum amylase and lipase in patients withchronic infective liver disease, especially in those having liver cirrhosis, may lead to anaccumulation of these enzymes in the blood.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-2568
    Keywords: LIVER ; HEAT SHOCK PROTEIN ; OXIDATIVE STRESS
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Heat shock proteins are intracellular proteinsassociated with a generalized response of cells tostress. The purpose of this study was to assess RNAlevels of heat shock protein 70 and 90 in fed or fasted rat livers during ischemia-reperfusion.Northern blot analysis of heat shock proteins wasperformed. Adenosine triphosphate and glutathione wereassessed. In baseline conditions, livers of fasted ratsshowed a twofold increase in mRNA for both heat shockproteins and 38% and 43% reductions in adenosinetriphosphate and glutathione, respectively, whencompared with organs from fed rats. After ischemia,livers of fasted rats presented a twofold decrease inheat shock protein mRNA, while no changes were observedin livers of fed rats; reduced glutathione and adenosinetriphosphate decreased 55% and 50% in fasted livers and 25% and 20% in fed organs,respectively. After 120 min of reperfusion, heat shockprotein mRNA rose threefold in fasted livers, while aslight decrease was observed in the fed group; reduced glutathione and adenosine triphosphate returnedto 65% and 70% of baseline values in fasted livers and85% and 90% in fed organs, respectively. In conclusion,the nutritional status affects heat shock protein expression determined by reperfusion. Thereduced antioxidant status leading to increasedoxidative stress could be the mechanism underlying thephenomenon.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1573-2568
    Keywords: hepatocyte ; ethanol ; cytosolic free calcium ; lactate dehydrogenase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The events implicated in the early phases of acute ethanol-induced hepatocyte injury and their relation with the nutritional status of the liver are not clearly defined. We aimed to determine the effect of ethanol on ATP and cytosolic free Ca2+ in hepatocytes isolated from fed or fasted rats. Cell injury was assessed by LDH release and trypan blue uptake, ATP by [31P]NMR spectroscopy, and cytosolic free Ca2+ with aequorin. In control conditions, cells from fasted animals had a lower ATP level (−52%) and a higher cytosolic free Ca2+ (+101%) than did those isolated from fed animals. Ethanol caused a dose-dependent cell injury in both groups. At all ethanol doses, greater damage occurred when using hepatocytes isolated from fasted rats. In both groups, a dose-dependent decrease in ATP content and a rise in cytosolic free Ca2+ were seen. The magnitude of these changes were significantly greater in the fasted group. In conclusion, these data showed that fasting affects the energy status and cytosolic free calcium level in hepatocytes; ethanol causes a dose-dependent cell injury that occurs in association with a fall in ATP and a rise in cytosolic free Ca2+ levels. The nutritional status of an animals is an important determinant of the severity of ethanol-induced damage to liver cells.
    Type of Medium: Electronic Resource
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