• Title of article

    Effect of Chronic Ethanol Consumption on Respiratory and Glycolytic Activities of Rat Periportal and Perivenous Hepatocytes

  • Author/Authors

    Baio، نويسنده , , Debra L. and Czyz، نويسنده , , Craig N. and Van Horn، نويسنده , , Cynthia G. and Ivester، نويسنده , , Priscilla and Cunningham، نويسنده , , Carol C.، نويسنده ,

  • Issue Information
    روزنامه با شماره پیاپی سال 1998
  • Pages
    8
  • From page
    193
  • To page
    200
  • Abstract
    Previous studies (Ivesteret al., Arch. Biochem. Biophys.322, 14–21, 1995) have established that periportal and perivenous hepatocytes isolated from ethanol-fed rats demonstrate lower ATP concentrations than those in control preparations when the cells are maintained at very low oxygen tension. In the present investigation, experiments were implemented with periportal and perivenous hepatocytes to determine the effects of chronic ethanol consumption on cellular respiratory and glycolytic activities, since both contribute to maintenance of the energy state of the liver cell. Both periportal and perivenous hepatocytes from ethanol-fed rats demonstrated significantly increased, rather than decreased, respiratory activity when monitored with oxygen concentrations ranging from 16 to 140 μM. Whole liver hepatocytes from control and ethanol-fed animals demonstrated equivalent oxygen utilization, however. Glycolytic activity, monitored by lactate + pyruvate concentrations obtained after both anaerobic and aerobic incubation protocols, was decreased in both cell types from ethanol-fed animals. The glycogen concentrations in freshly isolated periportal and perivenous hepatocytes were also decreased eight- and sevenfold, respectively, as compared with control preparations. Incubation under anaerobic conditions resulted in almost complete depletion of glycogen in both cell types. These observations suggest the possibility that the decreased energy state observed in hepatocytes from ethanol-fed animals is related to a depression in anaerobic glycolysis due to depletion of the endogenous substrate, glycogen.
  • Journal title
    Archives of Biochemistry and Biophysics
  • Serial Year
    1998
  • Journal title
    Archives of Biochemistry and Biophysics
  • Record number

    1611477