Human Platelet Senescence.
Abstract
Se-75 Selenomethionine was used as a cohort label, in vivo, in 3 volunteer patients. Platelets were isolated on various days during the study and the heavy and light platelet populations is lated. Kinetic data revealed that young platelets, released early from the bone marrow, were the heavy-large platelets, released early from the bone marrow, were the heavy-large platelets which progressed with age to lighter-smaller platelets. The glycolytic enzymes of the Embden-Meyerhof pathway have been analyzed in heavy-large (young) and light-small (older) platelets. The enclosed table reveals the Km and Vmax for each enzyme for the total platelet population and the Vmax for the individual platelet populations. When Vmax of the total platelet population is compared to glycolytic flux (glucose to lactate)., the apparent rate-limiting enzymes for glycolysis are phosphofructokinase and glyceral-dehyde-3-P-dehydrogenase. Several Embden-Meyerhof enzymes decreased significantly with age: hexokinase, phosphoglucomutase, phosphohexoseisomerase, phosphofructokinase, glyceral-dehyde-3-P-dehydrogenase, phosphoglyceromutase and lactic dehydrogenase. Since both phosphofructokinase and glyceraldehyde-3-P-dehydrogenase are also rate-limiting as well as significantly reduced with age--these two enzymes appear to be the critical enzymes in the modulation of in vivo human platelet senescence. Any attempt at preserving platelet viability on the self, might be directed towards stabilizing both of these enzymes.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jun 30, 1970
- Accession Number
- ADA955161
Entities
People
- Simon Karpatkin
Organizations
- NYU Langone Health