There is substantial evidence that oxidative stress participates in carcinogenesis (1-4). Oxidative stress, defined as an imbalance between reactive oxygen species (ROS) production and removal, results from the overproduction of ROS, decreased antioxidant defence or a combination of both. ROS-induced damage of macromolecules can lead to changes of their structure and, consequently, function. Oxidative damage of membrane phospholipids is called lipid peroxidation with malondialdehyde (MDA), an end-product of lipid peroxidation, being a widely used marker of cell exposure to oxidative stress (2-6). In addition, MDA is suggested to act as a tumor promoter and co-carcinogenic agent due to its high cytotoxicity (2, 3).