Potentially causal relationship between oxidative stress and cancer attracted much attention over the past several years since balance between pro-oxidant and antioxidant capacities is supposed to play an important role in cancer development. Reactive oxygen species (ROS) is a term usually reserved to describe group of highly reactive forms of oxygen carrying one or more unpaired electrons. They include superoxide anion, hydrogen peroxide, hydroxyl radical, singlet oxygen, etc. Surplus electrons, unused for generation of proton gradient, can interact with oxygen to produce superoxide. If not neutralized rapidly enough by the action of antioxidative enzymes and non-enzymatic antioxidants, the intracellular structures are damaged by oxidation. Source of ROS evoking oxidative stress is either exogenous or endogenous. The most important exogenous oxidants are ozone and cigarette smoke. Endogenously, numerous inflammatory cells, e.g. eosinophils, alveolar macrophages, etc., release ROS. However, mitochondria, more precisely protein complexes of the mitochondrial respiratory chain, are a dominant source of endogenous ROS. Pro-oxidant and antioxidant capacities in a healthy cell are kept in dynamic equilibrium by neutralizing overproduction of ROS and rebuilding of damaged intracellular structures. Clinical and experimental studies have provided sufficient background supporting an important role of oxidative stress in cancer development. Oxidative stress is related to cancer in multiple ways. First, oxidative stress can mediate oxidative damage to DNA and thereby initially promote carcinogenesis. Second, many malignant cells have an abnormal ability to cope with oxidative stress due to alterations in their antioxidant properties. One of the cancers with strongest link to oxidative damage and oxidative stress is head and neck squamous cell carcinoma since tobacco and alcohol as sources of massive quantities of ROS are clearly identified as etiologic factors of these malignancies. The authors present theoretical background of genesis and effect of oxidative stress in head and neck cancer. Furthermore, hypotheses of its impact on carcinogenesis are discussed.

        Key words: oxidative stress, antioxidative enzymes, head and neck cancer, carcinogenesis, reactive oxygen species, oxygen free radicals.