Inhibition of suicidal erythrocyte death by vitamin C
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OBJECTIVE: Similar to apoptosis of nucleated cells, suicidal death of erythrocytes is paralleled by cell shrinkage and cell membrane disorganization with phosphatidylserine exposure at the erythrocyte surface. Triggers of suicidal erythrocyte death include cell shrinkage, energy depletion, and oxidative stress, challenges at least partially effective by increasing the cytosolic Ca(2+) concentration. Apoptosis is inhibited by vitamin C. The present study thus explored whether vitamin C similarly influences suicidal erythrocyte death. METHODS: The cytosolic Ca(2+) concentration was estimated from Fluo3 fluorescence, phosphatidylserine exposure from annexin V-binding, and cell volume from forward scatter in fluorescence activated cell sorting (FACS) analysis. RESULTS: Energy depletion (48 h glucose removal) increased the cytosolic Ca(2+) concentration, decreased the erythrocytic cell volume, and enhanced annexin V-binding. Similarly, cell shrinkage by 48 h replacement of extracellular chloride with gluconate and oxidative stress (30 min exposure to 0.3 mM tert-butylhydroperoxide) triggered suicidal erythrocyte death as evident from enhanced annexin V-binding. Vitamin C (up to 0.28 mM) did not significantly modify the cytosolic Ca(2+) concentration, annexin V-binding, and cell volume in the absence of stressors stimulating suicidal erythrocyte death but significantly attenuated the suicidal erythrocyte death following cell shrinkage, energy depletion, and oxidative stress. CONCLUSION: Vitamin C is a potent inhibitor of suicidal erythrocyte death.
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