Captopril Induces Iron Release From Ferritin and Oxidative Stress

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Abstract
Captopril has been reported to possess reducing and iron-binding properties, which could favour iron delocalization from ferritin and oxidative stress. In the present paper, we have found that the drug was effectively capable of inducing a significant mobilization of ferritin iron, which was apparently superoxide anion-independent. Once released from ferritin as a result of captopril action, iron became free in the reduced form and could induce oxidant damage, as evaluated by deoxyribose-oxidative degradation. This phenomenon was not antagonized by the reported oxygen radical-scavenging properties of the drug. These data indicate that captopril is not always an antioxidant drug, and suggest that it may act as a pro-oxidant in the presence of ferritin in-vivo.