Plasma and erythrocyte enzymes in phenylhydrazine anemia.

SEVERAL YEARS AGO LaDue (2) made the iiiteresting observation that soon after myocardial infarction the plasma glutamic oxalacetie tramisammase is increased, reaches a peak within a few days, and then returns to normal. This observation stimulated a new area of clinical interest ill diseases related to infarction and necrosis as manifested ill plasma enzymes changes. The source of this increased plasma enzyme activity in disease has become of interest to the clinical chemist. Is this activity newly formed, or is the enzyme system transported from the necrotic tissue to the circulating plasma to be excreted or inactivated Experimental work has made it obvious that these enzymes are not excreted into tile urine. Where or how they are inactivated would he more difficult to demonstrate. Transport from necrotic tissue to plasma assumes that the “leaching” process transfers the complete kinetic system from the fixed tissue phase to the circulating plasma phase. The complexity of the problem is of course inherent in the complexity of protein structure and synthesis and the kinetics of the enzyme systems.