A ddition of untreated or glutaraldehyde-fixed human erythrocytes decreased hydrogen peroxide (H2O2)-mediated acute edematous injury in isolated rat lungs, H2O2-induced damage to cultured bovine pulmonary artery endothelial cells, and H2O2-dependent oxidation of reduced cytochrome C in vitro. The results suggest that intact erythrocytes can scavenge H2O2, and as a result, protect the lung and possibly other tissues from damage.