Some enzymologic aspects of the human erythrocyte

Abstract

The human erythrocyte engages solely in a glycolytic type of metabolic activity, a metabolic specialization which may be viewed as an expression of adaptive efforts directed toward survival in an environment rich in glucose, and in the face of a “handicap” due to the lack of a nucleus. Since relatively few biosynthetic reactions occur in erythrocytes, a specialized metabolic pathway, the Rapoport-Luebering cycle, has evolved in the human erythrocyte which provides a means of dissipating the excess of energy-rich phosphate so as to ensure continued glycolytic activity. Although anaerobic glycolysis constitutes the only important pathway for the catabolism of glucose in the human erythrocyte under normal physiological conditions, the cell is potentially capable of catabolizing glucose oxidatively as well as of metabolizing glucose by means of the uridyl transferase reaction sequence. The human erythrocyte is enzymatically equipped to oxidize glucose by way of the pentose phosphate metabolic cycle, but the alternate pathway of glucose catabolism can be activated only if the normally missing metabolic link to molecular oxygen is supplied. Partial activation can be achieved in the nonoxidative portion of the pentose phosphate cycle by supplying a suitable substrate. The glycolipoprotein-containing envelope of the human erythrocyte appears to perform an important metabolic function in regulating the flux of ions in and out of the cell and in controlling the flow of glucose and phosphate, both of which are essential metabolites for the human erythrocyte. Metabolic aberrations have been found in a variety of pathologic conditions, but only a few of these have been elucidated sufficiently to permit exact definition of the aberration. Most firmly established in the latter category are the metabolic aberrations found in drug-induced hemolytic anemia, in galactosemia and in hereditary spherocytosis.