Oxidative damage to DNA is the seemingly inevitable consequence of cellular metabolism. Furthermore, despite protective mechanisms, cellular levels of damage may increase under conditions of oxidative stress, arising from exposure to variety of physical or chemical insults. Elevated levels of oxidatively damaged DNA have been measured in numerous diseases, and as a result, it has been hypothesised that such damage plays an integral role in the aetiology of that disease.

Many epidemiological studies have reported inverse association between vegetable and fruit consumption and occurrence of cancer and other degenerative diseases. One of the possible mechanisms of this protective effect is by exerting antioxidative activities of such plant food constituents as vitamins A, C and E. These antioxidant vitamins are effective radical scavengers therefore they should protect biomolecules such as DNA from oxidative damage.

In our recently published works have been found that the levels of oxidative DNA damage in leukocytes were significantly higher while the concentrations of the antioxidant vitamins were significantly lower in colon and lung cancer patients than in control group. Moreover, the same direction of the changes has been found in patients with adenoma. This, in turn, suggests that the changes in aforementioned biomarkers of oxidative stress are characteristic for cancer development. Results of investigating relationship between oxidative DNA damage biomarkers and antioxidants in aging process will also be presented.

Although at present it is impossible to answer directly the question concerning involvement of oxidative DNA damage in etiology of different diseases it is likely that oxidative DNA base modifications may serve as a source of mutations that initiate carcinogenesis and other pathological conditions (i.e. they may be causal factors responsible for the process).

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1. Oxidative DNA damage; assessment and meaning in some human pathologies
2. Effects of basal level of antioxidants on oxidative DNA damage in humans
3. An involvement of mammalian MTH1 protein (8-oxo-dGTPase) in carcinogenesis and its potential utilization as a molecular marker of carcinogenesis and oxidative stress
4. Oxidative damage, DNA repair capacity and DNA repair gene polymorphisms and colon cancer.