The activities of the hepatic mitochondrial and microsomal total monoamine oxidase(MAO), and serum benzylamine oxidase were studied for cholestasis induced by common bile duct ligation and acute ethanol intoxication developed, or cholestasis
after
chronic ethanol intoxication for manifestation of the biochemical background of alcohol intoxication in hepatobiliary disease.
There were marked increases in the mitochondrial and microsomal total MAO activities of the liver in the rats treated with chronic ethanol intoxication, and showed a significant increase in the mitochondrial total MAO after treatment with acute
ethanol
intoxication.
When common bile duct was ligated in the rats, mitochondrial total MAO activity in the liver significantly decreased.
When common bile duct was ligated after chronic ethanol intoxication and acute ethanol intoxication was done after common bile duct ligation, the activity of the mitochondrial total MAO in the liver decreased more significantly than the group
only
with
ethanol intoxication was performed. However, the activity showed a higher degree on the same time points than the groups only with the common bile duct ligation.
The serum benzylamine oxidase ectivity in the group with only common bile duct ligation or the ethanol intoxication with cholestasis were measured between the 7th and 14th day, with no difference between two groups.
According to the above results, the hepatic MAO seems to be an enzyme in which its activity increases in acute and chronic ethanol intoxication. And total MAO in the liver is the enzyme with increased activity in ethanol intoxication with
cholestasis
more than in cholestasis. The cause of the increase is the development of biosynthesis. Accordingly, these results will be the data supporting that alcoholic drink is enzymologically harmful in hepatobillary disases.
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