To determine the zonal distribution of alcohol dehydrogenase in normal and cirrhotic human livers, we measured activities of this enzyme by quantitative cytochemical analysis along the liver cell plate in liver specimens from 10 normal organ donors and from 7 children with extrahepatic biliary atresia cirrhosis. In normal human liver samples, a continuous increase in alcohol dehydrogenase activity was observed along the sinusoid from the periportal to the perivenular hepatocytes (mean extinction units from 16.2 +/- 10.0 to 58.0 +/- 14.8). A similar observation was made in cirrhotic nodules, with activity increasing continuously from nodule periphery to center (7.6 +/- 4.1 to 44.9 +/- 13.3). This study demonstrates a heterogeneous pattern of alcohol dehydrogenase distribution along the sinusoid in normal human liver specimens. In addition, demonstration of this heterogeneity in human cirrhosis suggests that the cirrhotic liver is able to maintain a parenchymal functional organization, with persistence of metabolic zonation.
ABSTRACT. To evaluate whether liver metabolic zonation persists in human biliary cirrhosis, we used quantitative cytochemistry to measure activities of glucose 6 phosphatase (G6P) and NADPH dehydrogenase (ND) in hepatocytes situated in different zones of liver cirrhotic nodules. Liver specimens were obtained from 13 children with extrahepatic biliary atresia with compensated cirrhosis. Activity and distribution were compared with zonal activities measured in 17 control human liver specimens obtained during reduction hepatectomies for orthotopic liver transplantation. In normal human liver, G6P was 1.86 times more active in the periportal than in the perivenular zone. On the contrary, ND activity was lower in the periportal zone (63% of perivenular activity). A metabolic zonation persisted in extra-hepatic biliary atresia with compensated cirrhosis. G6P activity was 1.56 times greater at the nodule periphery than at the nodule center, whereas ND activity was lower at the periphery (75% of nodule center activity). This metabolic zonation is the opposite of that observed in animal toxic (CCL,) cirrhosis, in which greater G6P activity is observed at the nodule center and greater ND activity at its periphery. This confirms our previous hypothesis that the type of cirrhotic metabolic zonation may depend on the site of initial liver damage. (Pediatr Res 30: 286-289, 1991)
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