Subcellular fractionation of human platelets labeled with radioactive sodium chromate was utilized to study distribution and characterization of the 51Cr binding sites in these cells. The cytoplasmic fraction of the platelets contained the major portion of the radioactivity while microsomal and mitochondrial fractions played a minor role in the binding of chromate. The stromal sediment had approximately one third of the total radioactivity. Only about 20 per cent of the 51Cr taken up by the platelets was in a free ionic form and was in the cytoplasmic fraction. The major portion of the 51Cr in the platelets was bound to nucleotides in the platelet cytoplasm. Nucleotides of the α-granules had no radioactive chromate. Hypertonic media and platelet antiserum produced marked release of 51Cr from the platelets, whereas aggregating agents produced none.

In physiologic conditions, elution of 51Cr from labeled platelets is very limited because there is only little 51Cr in free ionic form in the cells. Release of considerable amount of 51Cr from the platelets can occur only in case of cell damage with release of nucleotides from the cytoplasmic pool. This was seen with hypertonic solutions and with platelet antibody. Platelet degranulation, as it occurs with aggregating agents, is not associated with release of 51Cr since the granular pool of nucleotides is not labeled by this compound.

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