High aspartate accumulation and defect of glutamate/aspartate transport in low potassium dog red blood cells

Abstract

The accumulation of Asp in low potassium (LK) dog red blood cells (RBCs) with defective Na-dependent (ND) glutamate (Glu)/aspartate (Asp) transport was examined. In RBCs with LK and defective ND-Glu/Asp transport (LK/GAT−), the amino acid influx defect appears to be specific to Glu/Asp, since influxes of the neutral amino acids alanine (Ala) and glutamine (Gln) were similar in both LK/GAT− RBCs and LK dog RBCs without the defect (LK/GAT+). Contrary to what might be expected with this transport defect, the Asp concentration in LK/GAT− RBCs was 10-fold higher than that in LK/GAT+ RBCs. Large, light RBCs separated by specific gravity were younger than small, dense RBCs in both LK/GAT− and LK/GAT+ RBCs. The youngest 10% of the cells had a 20% higher Asp concentration than the oldest 10% of the cells in both LK/GAT+ and LK/GAT− RBCs. The Glu and Gln concentrations decreased by 37%–47% as the cells aged, whereas Asp concentration decreased by 18%–19%. Therefore, the change in Asp metabolism during cell ageing might be smaller than the changes in the other amino acids. Thus, the Asp accumulation perhaps occurs at an early stage of cell development in LK/GAT− RBCs. The most likely cause of the Asp accumulation is a defect in Asp extrusion through ND-Glu/Asp transport.