Interactions Between Aflatoxin B sub(1) and Dietary Iron Overload in Hepatic Mutagenesis

Interactions between aflatoxin B sub(1) (AFB sub(1)) and dietary iron overload in hepatic were compared. Intracellular free ions were a catalyst for the formation of reactive oxygen and nitrogen species and consequently might cause oxidative damage to hepatocytes, DNA, protein, and lipids. The co-administration of iron and AFB sub(1) had a super additive effect on the generation of reactive oxygen and species and oxidative stress in the liver, as evidenced by the increased total lipid hydroperoxide concentration (LOOH) and the generation of 8OHdG. It was indicated that a high level of non-heme iron in hepatocytes could inhibit nitric oxide-induced apoptosis by converting nitric oxide from a pro-apoptotic molecule to an anti-apoptotic molecule. It was observed that the iron overload increased hepcidin production, which served to inhibit iron adsorption and its release into circulation from macrophages.