Free radicals and oxidative damage play important roles in aging and many
degenerative disorders such as cancer, cardiovascular diseases, and Alzheimer
disease. Antioxidants can alleviate some of the harmful effects of oxidative
damage. In this report, we describe that we have been using human red blood
cells (RBCs) as a model system to delineate the effects of oxidative damage on
human cells, particularly on glucose-6-phosphate dehydrogenase (G6PD)-
deficient human RBCs. By using a monolayer technique, we found that oxidative
dénaturation of hemoglobin leads to the release of hemin into the RBC
membrane and the released hemin is capable of oxidizing membrane proteins
via a thiyl radical intermediate as detected by the electron spin resonance technique.
By using a Laser Yiscodiffractometer (Vidometer) to measure RBC
deformability, we found that the deformability of G6PD-deficient RBCs
was drastically reduced by hydroxyl radicals. Perhaps as a consequence of
enhanced susceptibility to oxidative stress, G6PD-deficient individuals have
lower antioxidant levels, particularly vitamin C, than normal individuals.
Interestingly, we have also found that RBC deformability could be affected by
two environmental pollutants, namely, platinum and palladium, which can
enhance hydroxyl radical formation in the presence of hydrogen peroxide and
ferrous ion (Fenton reaction).