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KMID : 0371319840270040409
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Journal of the Korean Surgical Society
1984 Volume.27 No. 4 p.409 ~ p.420
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Effect of Hepatic Duct Ligation on Induction of Hepatic Changes by Aflatoxin B₁ in the Rat
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임근우/Lin, Keun Woo
김재성/강래성/김인철/김희규/Kim, Jai Sung/Kang, Rae Sung/Kim, Chul In/Kim, Hee Kyu
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Abstract
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It is well documented that aflatoxin, a metabolite of Aspergillus flavus, induce hepatocel-lular carcinoma in animals and has strong epidemiologic evidences related to malignant hepatoma in human being.
There are various factors modifying the induction of cancer by aflatoxin; protein - deficie-ncy diet and high vitamin A diet (Madhaven & Gopalan, 1965), and hormone such as estrogen (Newberne & Williams, 1969) and ACTH (Chedid et al., 1977).
Parenchymal changes and functional derangements of liver by such as viral hepatitis (Lin et al., 1974) and cirrhosis (Newberne et al., 1966) are also known as significant factors accelerating induction of hepatocellular carcinoma.
Clinically, bile stasis, cholangitis or biliary cirrhosis due to stones or parasitic disease in biliary tract, which is high in incidence and one of main surgical problems in Korea may secondarily_ caused hepatic cellular injuries.
To evaluate the effects of hepatic - injuries on induction of cancer by aflatoxin, authors made this experiments on rat.
Approximately one forth of hepatic parenchyme was surgically injured by means of double ligation and division of left extrahepatic bile duct.
Aflatoxin was administered into stomach through incubated oral tube.
Animals were divided into four groups: group with ligation of left hepatic duct and aflatoxin B1 administration, group with aflatoxin administration only, group with left hepatic duct ligation and dimethyl sulfoxide administration, group with left hepatic duct ligation and normal saline solution administration.
0.045mg/100gm of body weight of aflatoxin Bl was given for observation of early changes and 0.045mg/100gm of body weight/week, repeatedly up to 8 weeks for late changes.
Histological changes were studied on 2 days interval up to 9days for parenchymal changes of early stages and two weeks interval up to 10 weeks after last done of aflatoxin BI for
late changes.
For the histological analysis, hematoxylin-eosin stain, periodic acid Schiff reaction, van Gieson staining, methyl green pyronine staining, Masson´s trichrome staining and alkaline phosphatase staining were adopted.
The results were summarized as follows.
1) Mild degenerative and necrotic change´s of hepatocytes and slight proliferation of bile ductules were noticed in dimethyl surfoxide and saline treated group throughout experim-ental day.
2) Degenerative change and necrosis of hepatocytes were most prominent at fifth experimen-tal day, and these findings were repaired from seventh experimental day, but these find-ings were more severe in the group of aflatoxin administration with left hepatic duct liga-tion.
3) Regeneration of hepatocytes noted apparently from ninth experimental day, which was more prominent in aflatoxin administration group without left hepatic duct ligation than aflatoxin administration group with hepatic duct ligation.
4) Proliferation of bile ductule progressed with experimental day, and it were more remakable in aflatoxin administration with hepatic duct ligation group than aflatoxin without hepatic duct ligation group.
5) Micronodule formation appeared after two weeks of repeated doses of aflatoxin with left hepatic duct ligation group. This finding was more definite and increase in number and shape progression of duration. In repeated doses of aflatoxin without hepatic duct ligation group, this finding was noticed after six weeks of experiment, and less remarkable than left hepatic duct ligation group upto ten weeks.
With the results of this experiment that hepatic injuries duo to biliary occlusion accelerate the hepatotoxic effects and precancerous histologic changes of aflatoxin B1 significantly and rapidly, biliary occlusion from either inflammatory or mechanical origin might be a modify-
ing factor in induction of cancer by aflatoxin Bl.
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