**1. Introduction**

The redox status of cells is crucial for normal physiological functioning; however, when the prooxidant activity overrides the antioxidative capacity (AOC), oxidative stress occurs. Chronic oxidative stress causes cytotoxicity and organ failure. As such, it is believed to play a role in many diseases, such as cardiovascular, thromboembolic and neurodegenerative disorders, as well as aging [1].

In this review, we suggest that RBC, in addition to their primary role as oxygen and CO2 carriers, functions as redox modulators. Various RBC systems afford them with AOC that, in addition to balancing their own redox state, can provide antioxidative protection to the cellular and intercellular milieus throughout the body. Their vast number, mobility, and 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 by failing to neutralize oxidative stress. However, correcting

anemia, e.g., by repeated RBC transfusions or by 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.
