Iron and Hepatocellular Carcinoma

"Dietary iron overload and aflatoxin have a five-fold multiplicative
effect on mutagenesis"

Interactions between aflatoxin B1 and dietary iron overload in hepatic
mutagenesis
Toxicology, Volume 234, Issue 3, 20 May 2007, Pages 157-166
George A. Asare, Michelle Bronz, Vivash Naidoo, Michael C. Kew
Abstract
Background/aim
Dietary aflatoxin B1 (AFB1) exposure and iron overload are important
causes of hepatocellular carcinoma in sub-Saharan Africa. The aim of
this study was to investigate if the two risk factors have an
interactive effect.
Methods
Four groups of Wistar albino rats were studied for 12 months. Group 1
(control) was fed the normal chow diet; group 2 (Fe) was supplemented
with 0.75% ferrocene iron; group 3 (Fe + AFB1) was fed 0.75% ferrocene
throughout and gavaged 25 ìg AFB1 for 10 days; group 4 (AFB1) was
gavaged 25 ìg AFB1 for 10 days. Iron profile, lipid peroxidation
(LPO), 8-hydroxydeoxyguanosine (8OHdG), oxidative lipid/DNA damage
immunohistochemistry, superoxide/nitrite free radicals, cytokines IL6,
IL-10, transaminases (ALT/AST) and Ames mutagenesis tests were
performed.

Results
LPO and ALT showed a significant (p < 0.05)/additive effect and 8OHdG
a significant (p < 0.05)/multiplicative effect in the Fe + AFB1 group.
IL-6 produced a negative synergy as against an additive antagonistic
effect with IL-10. Massive deposits of 4-hydroxynonenal (4-HNE) and
8OHdG were observed in liver sections of the Fe + AFB1 group,
suggestive of multiplicative synergy. Significant levels of
mutagenesis (p < 0.001) were observed in the Fe + AFB1 group. This
multiplicative synergy was five-fold.

Conclusion
Dietary iron overload and AFB1 have a multiplicative effect on
mutagenesis


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