From oxidative DNA damage to molecular epidemiology

Abstract

Reactive forms of oxygen are released during normal respiration, by the oxidative burst of the macrophages in response to infection, and by a variety of exogenous environmental agents. Oxidative stress, caused by imbalance between the production of reactive forms of oxygen and their elimination, leads to oxidative damage of biomolecules. It is generally accepted that oxidative stress is involved either as cause or effect in a variety of human degenerative diseases. The antioxidant hypothesis proposes that natural antioxidants in fruit and vegetables scavenge free radicals before they can cause damage. To test the hypothesis a reliable biomarker for in vivo assessment of oxidative damage is needed which can be correlated with antioxidant levels on one hand and with disease on the other. Oxidative damage to lymphocyte DNA can be measured by the comet assay or by HPLC. This paper gives a brief review of the methods and their application both in in vitro and in in vivo studies dealing with mutagenesis and carcinogenesis. Molecular epidemiological studies in Slovakia concerning different disease states, aging and the role of diet, and antioxidant supplementation in prevention are reviewed as well.