| Popis: |
The intrusion of micromolar amounts of calcium into the calcium-poor interior of the human erythrocyte initiates a series of cataclysmic changes in cellular metabolism and morphology. These include (1) cellular shrinkage (elevated mean cell hemoglobin concentration), (2) loss of water and potassium, (3) rapid and near-total hydrolysis of intracellular ATP, (4) conversion of cell shape from biconcave disc to echinocyte and spheroechinocyte, (5) greatly diminished cellular deformability and elasticity, and (6) the accumulation of DAG. It has been suggested that this latter of phenomenon may account for the changes in cell shape and, perhaps, membrane viscoelastic properties. In the present study we have tested the hypothesis that DAG accumulation is important in the evolution of calcium-induced erythrocyte damage. Our results indicate that (1) calcium-loaded lamb erythrocytes become misshapen and inelastic but do not produce detectable DAG; (2) human red cells suspended in potassium-rich buffer do accumulate DAG after exposure to calcium and A23187 but do not become echinocytic or inflexible; (3) human erythrocytes artificially loaded with DAG are morphologically and elastically normal; and (4) human erythrocytes which have "naturally" accumulated DAG after prolonged incubation in the presence of calcium will retain this DAG after energy repletion. Despite marked elevations of DAG, these cells resume normal morphology and deformability. In aggregate, our data fail to support any direct role for DAG accumulation in the occurrence of calcium-induced damage to human erythrocytes. |
