| ironjustice@aol.com 2005-11-11, 5:52 pm |
| <<snip>>
the iron-supplemented diet showed grade 4 iron overload, comparable in
degree with that seen in patients with DIETARY iron overload
<<snip>>
J Pathol. 2005 Nov 8; [Epub ahead of print] Related Articles, Links
Iron-free neoplastic nodules and hepatocellular carcinoma without
cirrhosis in Wistar rats fed a diet high in iron.
Asare GA, Paterson AC, Kew MC, Khan S, Mossanda KS.
MRC/University Molecular Hepatology Research Unit, Department of
Medicine, university of the Witwatersrand and Johannesburg Academic and
Baragwanath Hospitals, South Africa.
Although excess hepatic iron in hereditary haemochromatosis and dietary
iron overload in the African causes hepatocellular carcinoma, it
usually does so in the presence of cirrhosis. A direct
hepatocarcinogenic effect of iron has not been proved. Moreover, an
animal model of hepatocellular carcinoma induced by iron overload has
not been available. The aim of this study was to develop such a model
and to use it to ascertain whether excess hepatic iron is directly
hepatocarcinogenic. Sixty Wistar albino rats were fed a chow diet and
60 the same diet supplemented initially with 2% carbonyl iron for 12
months, followed by 0.5% ferrocene for 20 months. Five rats from each
group were sacrificed every 4 months for 24 months for histological and
biochemical monitoring. By 16 months, hepatocytes in all the rats
receiving the iron-supplemented diet showed grade 4 iron overload,
comparable in degree with that seen in patients with advanced
hereditary haemochromatosis and dietary iron overload. Altered hepatic
foci and pre-neoplastic nodules were first seen at 16 months. These
increased in size and number with time, were iron-free, stained
positively with placental glutathione sulphydryl transferase, and
showed the same histological features as the iron-free foci described
in patients with hepatocellular carcinoma complicating hereditary
haemochromatosis. At 32 months the eight surviving rats in the iron
overloaded group were sacrificed. The livers of five of these rats
contained pre-neoplastic nodules and one showed, in addition, an
iron-free, well-differentiated hepatocellular carcinoma. The tumour
stained positively for placental glutathione sulphydryl transferase.
Neither cirrhosis nor portal fibrosis was present in this or any
iron-loaded animal. We conclude that hepatocellular carcinoma may
complicate dietary hepatic iron overload in Wistar albino rats in the
absence of fibrosis or cirrhosis, confirming an aetiological
association between dietary iron overload and the tumour and suggesting
that iron may be directly hepatocarcinogenic. Copyright (c) 2005
Pathological Society of Great Britain and Ireland. Published by John
Wiley & Sons, Ltd.
PMID: 16278820 [PubMed - as supplied by publisher]
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