Insulin Reduces Eryptosis in Thalassemic Red Blood Cells

Abstract

Eryptosis, a form of programmed cell death in red blood cells, is triggered by oxidative stress or energy depletion. Modulation of mechanisms regulating energy supply or oxidative stress impacts eryptotic behavior of red blood cells. In thalassemic blood cells enhanced eryptosis causes anemia. Insulin enhances the flux of glucose by stimulating glycolysis to produce ATP and NADH in human erythrocytes. Thalassemic red blood cells are prone to undergo eryptosis leading to anemia. This paper gives evidence that the stimulatory effect of insulin leads to a protection of oxidative-stress-induced eryptosis, especially in red blood cells of thalassemic donors. Oxidative stress in thalassemic red blood cells was induced by tert-butylhydroperoxide (tBOOH) with or without supplementing the media with insulin. Phosphatidylserine exposure, measured as annexin V-binding, was used as a marker for eryptosis in thalassemic red blood cells. Insulin significantly decreased (P<0.05) the percentage of phosphatidylserine exposing red blood cells in thalassemic red blood cells.