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The primary purpose of the Red Blood Cell (RBC) is to transport Oxygen from the lungs to the tissues.
However, hemoglobin also undergoes a continuous slow autoxidation reaction whereby the Fe(II) heme is
oxidized to Fe(III) heme and the bound oxygen is reduced to superoxide, which initiates an oxidative cascade
reaction involving the production of various reactive oxygen species (ROS). This process is dramatically enhanced
for partially oxygenated hemoglobin present in the microcirculation where oxygen is being transferred to the
tissues. Although this reaction involves only a small fraction of the hemoglobin, considering the large pool of
RBCs, it is a source of ROS that cannot be neglected. The actual transfer of ROS from the RBC to lung capillary
venules under hypoxic conditions and the resultant inflammatory response has been demonstrated by rat and
mice studies. In order to evaluate potential pathophysiological affects of RBC oxidative stress we have developed
a method to evaluate the extent of RBC oxidative stress. During the autoxidation reaction, a fraction of the nonneutralized
ROS attacks the heme producing fluorescent heme degradation products. These products are found in
all blood samples and reflect an integrated measure of RBC oxidative stress. We have shown that certain diseases
like sickle cell disease are associated with an increase in RBC oxidative stress. These studies indicate that oxidative
stress originating from the RBC contributes to the pathology associated with certain diseases.
Biography
Joseph M. Rifkind completed his Ph.D. in physical chemistry from Columbia University in 1966. He has been at the National Institutes of
Health since 1968. Since 1985 he was the Chief of the Molecular Dynamics Section at the National Institute on Aging. He has published
over 130 papers in peer reviewed journals and over 20 book chapters. His research has been directed at the physiological role of
oxidative stress and nitric oxide metabolism primarily involving the red blood cell with 8 papers dealing with amyloids and Alzheimer�s disease.
Joseph M. Rifkind
National Institute on Aging, USA
rifkind@verizon.net
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