Oxygen radicals and tissue damage in heart hypertrophy

Cyanide-resistant respiration in heart homogenates supplemented with 1 mM NADH was greater in hypertrophied homogenates (60 days banding) with respect to control homogenates, particularly when the homogenates were incubated in 100% oxygen. The intermyofibrillar mitochondria from hypertrophied hearts produced more superoxide radicals than sub-sarcolemmal mitochondria, and both values were greater than in the unbanded group. H2O2 formation was more evident in the intact mitochondria prepared from hypertrophied hearts than in those of the control hearts. Moreover, the perfusion of isolated hearts in anoxic and reoxygenated conditions caused a greater lipoperoxidative and functional damage at the mitochondrial level in hypertrophied hearts than in the control hearts. These results, correlate with the reduction in mitochondrial function found in the overloaded hearts, suggest an involvement of the reactive species of oxygen in the formation of cardiac damage induced by prolonged aortic banding.