Our results elucidating the mechanism of extracellular Hb-induced oxidative damage to the mitochondrial respiratory chain will contribute to better understanding of some of the underlying pathophysiology of pulmonary arterial hypertension caused by cell free Hbs; and, in addition, lend new insight into potential antioxidative therapeutic interventions in hemolytic diseases. This evidence concerns the gene GSTM1 and pulmonary arterial hypertension.