Abstract
The RBC from mice of certain inbred strains hemolyzed under oxidative stress (2.0 mmol/L hydrogen peroxide), whereas red cells from mice of other strains did not. In the experimental system human erythrocytes did not hemolyze. The rate of formation of malonyldialdehyde (a fatty acid oxidative breakdown product) was fourfold higher in hemolytic v nonhemolytic red cells. There was insufficient variation in the levels of glutathione, peroxidase activity or its substrate, reduced glutathione, to explain these hemolysis differences. On the other hand, the antioxidants butylated hydroxyanisole and hydroxytoluene, and histidine protected the hemolysis-prone red cells from breaking open. The hemolysis trait demonstrated autosomal recessive Mendelian inheritance. When using inbred, recombinant inbred, and congenic inbred mice, this hemolysis/nonhemolysis trait correlated 1:1 with the type of hemoglobin beta chain in the RBC. This experimental system is a potential model for investigating the role of hemoglobin in prehemolytic events.
