PMID: 9534206Apr 16, 1998Paper

Aflatoxin exposure produces serum alphafetoprotein elevations and marked oval cell proliferation in young male Pekin ducklings

Pathology
S SellH A Dunsford

Abstract

Feeding of aflatoxin to ducks produces extensive oval cell proliferation in the liver associated with a prolonged elevation of serum alphafetoprotein (AFP). Short term feeding of 0.075-0.6 microgram/g of aflatoxin to young male Pekin 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 microgram/g and 0.3 microgram/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.

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Citations

Jan 23, 1999·Current Opinion in Cell Biology·M Alison
Dec 15, 2011·Biochemical and Biophysical Research Communications·Young Ju Lee, Seong-Wook Lee
Dec 23, 2009·Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association·Mosaad A Abdel-WahhabFathia A Mannaa
Jan 4, 2006·Journal of Applied Toxicology : JAT·Mosaad A Abdel-WahhabMohamad M Hagazi
Nov 28, 2012·Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology·Clarinda ChuaHan-Chong Toh
Oct 17, 2017·Journal of Cellular Physiology·Mohammad MohajeriAmirhossein Sahebkar
Jun 5, 2002·World Journal of Gastroenterology : WJG·Meng-Sen LiGang Li
May 29, 2018·Tumour Biology : the Journal of the International Society for Oncodevelopmental Biology and Medicine·Zoran IlicStewart Sell
Apr 17, 2013·Toxicology and Industrial Health·D Senthil KumarN Anitha

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