**7. Conclusions**

The redox state is crucial for physiological functioning of cells, but excess reactive oxygen and nitrogen species causes oxidative stress, which is associated with many diseases, including hemolytic anemia. These anemias are characterized by accelerated destruction (hemolysis) of mature RBC and their precursors that is not balanced by compensatory overproduction. Although oxidative stress is not the primary etiology of most of these anemias, it mediates many of their symptoms. The main function of RBC is oxygen transport, for which they have evolved efficient nonenzymatic and enzymatic antioxidative systems for protection against oxidizing substances to which they are exposed. These systems serve mainly the RBC requirements, but may influence other neighboring cells as well, making the RBC antioxidative protective agents of the cellular and intracellular milieus throughout the body. Their vast number, mobility, occurrence throughout the body and renewability make them good candidates for this function. A decrease in their number (anemia) or function may exacerbate the symptoms of many diseases, including hemolytic anemias, by failing to neutralize oxidative stress. However, correcting anemia, e.g., by repeated RBC transfusions or iron supplementation, may increase the iron load, which, in turn, causes oxidative stress. This situation suggests that the status of both iron and redox should be monitored during treatment, using RBC as bioindicators and using flow cytometry multiparameter analysis.
