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Metabolic activation of aflatoxin B 1 to aflatoxin B 1 ‐8,9‐epoxide in woodchucks undergoing chronic active hepatitis
Author(s) -
GemechuHatewu Mekonnen,
Platt KarlLudwig,
Oesch Franz,
Hacker HansJörg,
Bannasch Peter,
Steinberg Pablo
Publication year - 1997
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19971114)73:4<587::aid-ijc21>3.0.co;2-5
Subject(s) - aflatoxin , woodchuck hepatitis virus , carcinogen , hepatitis b virus , mycotoxin , hepatocellular carcinoma , hepadnaviridae , hepatitis , hepatitis b , liver cancer , biology , virus , virology , medicine , immunology , biochemistry , food science
Chronic hepatitis B virus infection as well as consumption of food contaminated with the mycotoxin aflatoxin B 1 are considered to be 2 major risk factors for the development of primary liver cancer in humans. Furthermore, epidemiological surveys indicate that hepatitis B virus and aflatoxin B 1 might act synergistically to induce primary liver cancer. In the present study, we have tested the hypothesis that the metabolic activation of aflatoxin B 1 to aflatoxin B 1 ‐8,9‐epoxide, the ultimate mutagenic and carcinogenic mycotoxin metabolite, is enhanced in an experimental model of chronic hepatitis using woodchucks, chronically infected with the woodchuck hepatitis virus. Woodchuck liver microsomes were incubated with radiolabeled aflatoxin B 1 , the resulting aflatoxin B 1 ‐8,9‐epoxide was trapped as a glutathione conjugate and its formation rate was determined by a reversed‐phase HPLC analysis. In woodchuck hepatitis virus‐positive woodchucks, activation of aflatoxin B 1 to aflatoxin B 1 ‐8,9‐epoxide was reduced when compared to woodchuck hepatitis virus‐free animals, and the extent of the reduction was dependent on the severity of the hepatitis. Hence, at least in woodchucks, a chronic hepadnaviral infection does not lead to an enhanced activation of aflatoxin B 1 . Int. J. Cancer 73:587–591, 1997. © 1997 Wiley‐Liss, Inc.