Author
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SELL, STEWART - UNIVERSITY OF TEXAS |
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XU, KAI-LI - UNIVERSITY OF TEXAS |
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Huff, William |
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Kubena, Leon |
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Harvey, Roger |
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DUNSFORD, HAROLD - UNIVERSITY OF TEXAS |
Submitted to: Pathology
Publication Type: Peer Reviewed Journal Publication Acceptance Date: 8/1/1997 Publication Date: N/A Citation: N/A Interpretive Summary: A toxin produced by fungi (molds) named aflatoxin is extremely toxic to animals and humans. Aflatoxin is a known cancer-causing agent and is a concern to both animal and human health because of it is a frequent contaminant of animal feeds and human foods. When aflatoxin was fed to ducks for a short period of time certain cells in their livers under went changes that are indicative of early stages of cancer induced by chemicals. When ducks were fed aflatoxin for a long period of time a certain blood protein was increased. The presence of this protein in the blood as well as cell proliferation are markers (indicators) of early events in the development of liver cancer. These data suggest that the high incidence of liver cancer in some areas of the world may be attributed to the consumption of aflatoxin contaminated water and foods. Technical Abstract: Feeding of aflatoxin to ducks produces extensive oval cell proliferation in the liver associated with prolonged elevation of serum alphafetoprotein (AFP). Short term feeding of 0.075-0.6 ug/g of aflatoxin to young male Perkin ducks results in rapid and massive dose-related proliferation of "oval" cells, which extend from the portal zone across the hepatic lobule within three to five weeks. Longer term feeding of 0.15 ug/g and 0.3 ug/g results in prolonged elevations of serum AFP. Prolonged elevation of serum AFP serves as a marker of oval cell proliferation preceding hepatocellular carcinoma (HCC) development. These results confirm that ducks are sensitive to low amounts of aflatoxin and develop early lesions that have been shown in other studies to be associated with hepatocarcinogenesis. These findings in ducks support the likelihood that aflatoxin exposure contributes to the risk for development of HCC in humans. |