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LYSIS OF VITAMIN E‐DEFICIENT RAT ERYTHROCYTES BY RAT LIVER MICROSOMES IN AN NADPH‐DEPENDENT PROCESS IN THE PRESENCE OF INHIBITORS OF LIPID PEROXIDATION
Author(s) -
Willis Roger J
Publication year - 1983
Publication title -
australian journal of experimental biology and medical science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0004-945X
DOI - 10.1038/icb.1983.13
Subject(s) - microsome , lipid peroxidation , hemolysis , lysis , biochemistry , haemolysis , hemolysin , chemistry , nadph oxidase , vitamin e , oxidase test , vitamin , red blood cell , enzyme , biology , antioxidant , immunology , virulence , gene
Summary Haemolytic substances are generated by rat liver microsomes undergoing NADPH‐dependent lipid peroxidation. In the present experiments, vitamin E‐deficient red cells were found to be haemolysed in an NADPH‐dependent process by rat liver microsomes in the presence of EDTA, an inhibitor of microsomal lipid peroxidation. This is in contrast to the behaviour of normal, vitamin E‐adequate red cells which are resistant to lysis under similar conditions. Aminopyrine (AP), a substrate for the microsomal mixed function oxidase system, was found to prevent lysis of vitamin E‐deficient red cells in NADPH‐microsome‐EDTA mixtures. Experiments designed to detect only the more stable haemolysins forMed. in such mixtures involved sampling and assaying for haemolytic activity in the presence of AP. The results support the conclusion that haemolysis was due to a short‐lived species. If EDTA is omitted from the NADPH‐microsome mixture other more stable haemolysins are produced.