Oxidative damage induced by the generation of reactive oxygen species (ROS) is thought to be related to human cancer aetiology. Oxidative stress can result in DNA damage, including oxidized bases, formation of DNA adducts and DNA strand breaks, as well as lipid peroxidation, protein modification, membrane disruption and mitochondrial damage. The effect of reactive oxygen species is balanced by the antioxidant action ofnonenzymatic antioxidants (e.g. vitamins A, C, E, glutathione and flavonoids), as well as antioxidant enzymes. There are three main types of antioxidant defence enzymes: superoxide dismutases, catalase and glutathione peroxidases. A variety of cancer cells are known to have lower antioxidant enzyme activity when compared with their normal counterparts. Many studies have examined genetic variation in the genes coding for these enzymes and their relationship to cancer risk. Only a few genetic variants (single nucleotide polymorphisms--SNPs) in genes related to antioxidant defence were found to be associated with breast, prostate, lung, pancreatic, colorectal and bladder cancer. However, the results from these have been contradictory. Moreover, it is believed that environmental as well as genetic factors are implicated in the development of cancers, and consequently it is important to assess both genetic (including gene-gene association) and non-genetic (e.g. diet, supplementation, smoking and alcohol consumption) variability in the activities of defence enzymes in relation to cancer. In this review we focus on the biological function of antioxidant defence enzymes, and relationship between well-known SNPs in SOD1, SOD2, CAT, GPX1 and GPX4 genes and genetic susceptibility to cancer.