Oxidative processes in red blood cells from normal and diabetic individuals.

The oxidation processes in normal and diabetic erythrocytes after cell exposure to H2O2 and t-butyl hydroperoxide, as well as the effect of malondialdehyde (a stable end product of lipid peroxidation) on erythrocyte membrane structure and stability were studied. The malondialdehyde level began to increase only after oxidation of most of the red blood cell glutathione by peroxides. The activation energy of malondialdehyde was 53 +/- 7 kj/mol. Sodium azide inhibited the oxidation processes induced by t-butyl hydroperoxide. The modification of erythrocytes by malondialdehyde decreased the fluidity of the membrane lipid bilayer measured by fluorescence anisotropy and increased the osmotic stability of the cells. The level of endogenous thiobarbituric acid-reactive species was higher and antioxidative activity was lower in diabetic cells. It seems likely that oxidation processes and accumulation of malondialdehyde can contribute directly to changes in the properties of ¿diabetic¿ red blood cells and may cause the development of long-term complications.