[The new face of factors induced by hypoxia--HIF-1 and HIF-2 and oxidative stress].

Studies on the mechanisms of adaptation to adverse hypoxic conditions led to the discovery of hypoxia inducible factors, HIF-1 and HIF-2. These factors regulate the expression of many genes which allow cells to adapt to changes in oxygen concentration and counteract the effects of oxidative stress developing in hypoxia. Regulation of HIF activity is dependent on the prolyl hydroxylases activity and results in its degradation under normoxic conditions by the ubiquitin-dependent proteasome pathway. Recent studies indicate a specific role of reactive oxygenspecies (ROS) generated by the mitochondrial respiratory chain in regulation of HIF stability. ROS affect also the level of nitric oxide (NO), leading to a reduction in its concentration by forming reactive nitrogen species (RNS), which may cause the increase in oxidative and nitrosative stress. Regulation of HIF activity by ROS, NO and RNS is currently the subject of many studies and seems to be a mechanism dependent on conditions (e.g., normoxia/hypoxia), or concentrations of individual stimulators (e.g. NO donor used).