Alcohol dehydrogenase (ADH) activity was found to be present principally in liver tissue in the rat although significant activity was detected in the mucosa of the stomach and small intestine. Following hepatocellular injury induced by carbon tetrachloride, ADH was detected in plasma and bile. Biliary excretion of ADH rose shortly after liver injury was induced. The interruption of bile excretion by bile-duct ligation following hepatic parenchymal-cell injury resulted in significantly higher plasma ADH activity suggesting that ADH had been diverted from bile to blood. In contrast GOT and LDH did not appear to be released into bile after hepatocellular injury. These physiological observations provide an explanation for the clinical findings that plasma ADH is present in highest activity in patients with liver-cell necrosis and intrahepatic cholestasis.
|Original language||English (US)|
|Number of pages||9|
|Journal||The Journal of laboratory and clinical medicine|
|State||Published - May 1 1968|
ASJC Scopus subject areas
- Pathology and Forensic Medicine