Description: Oxygen reactive free radicals, more known as reactive oxygen species (ROS) have dual nature. On the one hand, they necessary for normal function of the cell, but on the other side when ROS is in excess can be mediators of damage to cell structures and this harmful effect is termed oxidative stress. The organism counteracts to ROS by the action of enzymatic and non-enzymatic antioxidants systems, such as trying to maintain redox balance. Although the effect of antioxidant protection, oxidative damage accumulates during the life cycle and is common for many types of cancer cell that are linked with altered redox regulation of cellular signaling pathways. Also and radical-related damage to DNA, to proteins and to lipids are suggested to play a main role in the progress of age-dependent diseases such as cancer, arteriosclerosis, neurodegenerative disorders and other conditions. This review examines the evidence for involvement of the oxidative stress in the carcinogenesis process. Attention is focused on chemical and biochemical aspects of free radicals, the endogenous and exogenous sources of their generation, the DNA damage, the damage to lipids and proteins by free radicals and the mechanisms of carcinogenesis