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Fanconi Anemia (FA) is an autosomal recessive disease of childhood. However, the FA pathway is responsible for the development of leukemia and the other cancers. It has been also demonstrated that FA, an only human genomic instability syndrome is very sensitive to oxidative stress and ROS overproduction. In the present work, we consider major mechanisms of antioxidant protection in FA cells. We showed that there are two types of such mechanisms: the suppression of ROS overproduction by FA genes through the activation of basic FA anemia proteins under the conditions of oxidative stress and the application of free radical scavengers able to react with iron-dependent ROS such as flavonoids rutin and quercetin. The last nontoxic compounds of vitamin P group might be recommended for the treatment of FA anemia patients. Then, we discussed the role of FA anemia proteins in cancer development.