Carcinogenesis, Vol 18, 599-603, Copyright © 1997 by Oxford University Press
P Carthew, BM Nolan, AG Smith and RE Edwards
Diethylnitrosamine (DEN) was administered to rats as a single dose, which
is known not to give rise to liver tumours without subsequent promotion.
Iron dextran (Fe/Dex) was then administered parenterally to the animals, to
induce iron overload. At 3 and 6 months after the final Fe/Dex treatments,
livers were examined quantitatively for the numbers of the placental form
of glutathione-S-transferase (GST-P) expressing foci, the area occupied by
these foci and their size distribution. The results demonstrate that iron
not only increased the number of foci after DEN initiation in the rat
liver, but that the area occupied by these lesions increased significantly
between 3 and 6 months after initiation. There is no evidence that iron
increased the number of GST- P expressing foci present in rats not exposed
to DEN. This indicates that iron did not act as an initiator in this rodent
model of liver cancer. The increase in the area of the liver occupied by
the foci in iron and DEN treated rats was due to an increase in the size of
the foci, as well as to an increase in the number of foci. This is the
first demonstration that iron can act as a promoter of DEN initiated
hepatocytes. It also demonstrates that fibrogenesis is not an absolute
requirement for the promotion, by iron, of liver foci in the rat, and that
this could also be the case for iron overload in man. Iron may also act as
a promoter of already initiated hepatocytes in the development of human
liver cancer, as it does in the rat.
ARTICLES
Iron promotes DEN initiated GST-P foci in rat liver
MRC Toxicology Unit, University of Leicester, UK.
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