It appears that the presence of labile iron pool (LIP, iron not bound to proteins) in cells can result in the production of reactive oxygen species namely COH radical which may be responsible for the formation of 8-oxo-7,8-dihydro- 2N-deoxyguanosine (8-oxodG) in the cellular DNA. This oxidatively modified molecule is regarded as a good biomarker of cancer risk and a general index of oxidative stress in relation to other diseases. There are numerous data suggesting that oxidative stress may be involved in the development of cardiovascular diseases and cancer. It has been observed that heterozygosity for hereditary hemochromatosis (a disease with abnormal iron storage) is a risk factor for vascular diseases. Previously we have demonstrated higher levels of LIP in a group of atherosclerotic patients when compared with the control group. This suggests that LIP may increase the risk of disease development. The aforementioned condition may lead to oxidative stress, which is manifested by a higher level of 8-oxodG in blood lymphocytes, and may be one of the factors responsible for the development of cardiovascular diseases. We have also reported the relationship between LIP and the endogenous level of 8-oxodG in human lymphocytes of the colon cancer patients. Good correlation has been determined between LIP and oxidatively modified nucleoside. The results of our studies on piglets supplemented with iron dextran (FeDex) also show an increase in the 8-oxodG level in hepatic DNA. These findings confirm the possibility that iron overload may favor the persistence of harmful LIP which may catalyze generation of the potentially carcinogenic 8-oxodG moiety in the cellular DNA.