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NADPH-dependent microsomal lipid peroxidation and the problem of pathological action at a distance

1978; Elsevier BV; Volume: 27; Issue: 4 Linguagem: Inglês

10.1016/0006-2952(78)90373-8

1873-2968

Mark K. Roders, Eric A. Glende, Richard O. Recknagel,

Vitamin C and Antioxidants Research

Lipid peroxidation occurs in vitro in a system consisting of rat liver microsomes and NADPH. If a small quantity of red cells is added, they will hemolyze. Lipid peroxidation (i.e. malonic dialdehyde evolution) always precedes red cell hemolysis in our system. This finding is contrary to earlier experiments of others, in which much higher concentrations of red cells were used, and in which certain other conditions varied from those used in our work. Addition of EDTA, which prevented lipid peroxidation, completely prevented red cell hemolysis. When aminopyrine was added, there was vigorous production of formaldehyde and neither lipid peroxidation nor red cell hemolysis occurred. Neither malonic dialdehyde nor hydrogen peroxide is responsible for the red cell hemolysis. If EDTA and erythrocytes are added to a microsomal system that has a prior history of NADPH-induced lipid peroxidation, the erythrocytes show prelytic damage, which can be detected by an osmotic fragility test. If erythrocytes are added to a system in which microsomal lipid peroxidation has been prevented (by the presence of EDTA), there is no evidence of osmotic fragility. These experiments suggest that some product or products arising in the peroxidizing microsomal lipids are capable of producing red cell damage.