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Mitochondrial adenosine triphosphatase activity of hepatocytes in obstructive jaundice
Author(s) -
Ker ChenGuo,
Sheen PaiChing
Publication year - 1995
Publication title -
journal of hepato‐biliary‐pancreatic surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.63
H-Index - 60
eISSN - 1868-6982
pISSN - 0944-1166
DOI - 10.1007/bf02349260
Subject(s) - atpase , medicine , cholestasis , jaundice , adenosine triphosphatase , pi , endocrinology , triphosphatase , common bile duct , mitochondrion , enzyme , ligation , chemistry , mole , gastroenterology , biochemistry , biology
The activity of adenosine triphosphatase (ATPase) in the mitochondria of hepatocytes in extrahepatic cholestasis was studied calorimetrically. Elevation of Na + ‐K + ‐ATPase, Ca 2+ ‐ATPase, and Mg 2+ ‐ATPase activities in the mitochondria of hepatocytes was found in rats after bile duct ligation. Peak activity levels of these three enzymes were found in the group that had been ligated for 7 days. The activities were found to be extremely high in rats in very poor physical condition and with very poor motor activity 7 days after ligation. In a clinical study, these activities were examined in 44 patients classified into three groups: group I, those with non‐jaundice cholelithiasis; group II, those with obstructive jaundice caused by common bile duct stones, and group III, those with obstructive jaundice caused by extrahepatic malignancy. All patients were operated on and liver specimens were collected for study. Na + ‐K + ‐ATPase activity was 0.86±0.18, 1.87±0.40, and 1.92±0.32. (M±SE) μmole pi/mg protein per hour for groups I, II, and III, respectivety. Mg 2+ ‐ATPase activity was 0.86±0.18, 1.87±0.34, and 1.50±0.35 μmole pi/mg protein per hour for groups I, II, and III. Ca 2+ ‐ATPase activity was 1.01±0.26, 2.51±0.44, and 2.08±0.51 μmole pi/mg protein per hour for groups I, II, and III. The values in groups II and III were significantly higher than those in group I. Elevation of these ATPase activities was clear in obstructive jaundice. These results may be due to the disturbed metabolism of hepatocytes or even to the cessation of metabolism, and hepatocytes try to reach a compensatory status during cholestasis.