CAPTOPRIL INDUCES IRON RELEASE FROM FERRITIN AND OXIDATIVE STRESS

Captopril has been reported to possess reducing and iron-binding prope rties, which could favour iron delocalization from ferritin and oxidat ive stress. In the present paper, we have found that the drug was effe ctively capable of inducing a significant mobilization of ferritin iro n, which was apparently superoxide anion-independent. Once released fr om ferritin as a result of captopril action, iron became free in the r educed form and could induce oxidant damage, as evaluated by deoxyribo se-oxidative degradation. This phenomenon was not antagonized by the r eported oxygen radical-scavenging properties of the drug. These data i ndicate that captopril is not always an antioxidant drug, and suggest that it may act as a prooxidant in the presence of ferritin in-vivo.