Abstract
Summary
1. Pretreatment of fatty acid with human plasma, plasma albumin or globulin, unesterified cholesterol, or cyanide retards or prevents hemolytic activity. Once lytic quantities of fatty acid are bound by human erythrocytes, the above substances reverse their protective activity and accelerate hemolysis. 2. Plasma and plasma factors appear to accelerate intrinsic oleate hemolytic activity rather than act via a secondary superimposed lytic mechanism; the mode of cyanide action is unknown. 3. The oleate hemolysis protective and accelerating properties of human plasma can be inhibited progressively and simultaneously by pretreatment with oleate. Both mechanisms appear to depend upon plasma ability to bind fatty acid. 4. The intensity of oleate hemolysis acceleration by human plasma or plasma fractions is not uniform. Variations can be attributed to differences in fatty acid binding capacities and to inhibitors which possess unesterified fatty acid activity. 5. A hypothesis is suggested for linking increases in mammalian plasma unesterified fatty acid with in vivo hemolysis.
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