A comparative evaluation of oxidative status of erythrocytes in normal and sickle cell disease patients
It is well established that G6PD deficient individuals are subjected to high oxidative stress and, hence, stiffening of the cell membrane due to oxidation of important membrane proteins. This effect is pronounced in RBCs where G6PD is the sole producer of NADPH, an essential cofactor in the antioxidant defense mechanism. A different approach is to evaluate oxidative stress as the analysis of antioxidant concentrations. GSH can be oxidized, mainly to glutathione disulfide (GSSG), or can form glutathionylated proteins (PSSG). The measurement of GSG, GSSG give fundamental information on the intracellular redox status. Analytical methods based on spectrophotometry, HPLC, capillary electrophoresis, nuclear magnetic resonance, and mass spectrometry have been reported for the determination of glutathione in biological samples. Our study has concluded that the HPLC method to measure the concentration of reduced (GSH) and oxidized (GSSG) glutathione in the normal (healthy) and Sickle Cell Disease patients. Erythrocyte glutathione depletion has been linked to hemolysis and oxidative stress. Our study revealed that the total antioxidant status in steady-state sickle cell disease (SCD) patients and compared it with some healthy individuals and related it to certain hematological parameters and their recent clinical history. 15 (males & females) adult SCD patients and 15 age-matched controls were studied. And we hypothesized that altered glutathione and glutamine metabolism play a role in this process. Total glutathione (oxidized & reduced) were assayed in erythrocytes of 15 SCD patients and 15 healthy volunteers. Erythrocyte glutathione levels were significantly lower in SCD patients than in healthy volunteers. The ratio of erythrocyte GSH: GSSG correlated inversely to the oxidized levels of the erythrocytes.
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Enika Nagababu, Mary E. Fabry, Ronald L. Nagel and Joseph M. Rifkind. Heme Degradation and Oxidative Stress in Murine Models for Hemoglobinopathies: Thalassemia, Sickle Cell Disease and Hemoglobin C Disease. Blood Cells Mol Dis. 2008; 41(1): 60-66.
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