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Red blood cell phagocytosis and lysis following oxidative damage by phenylhydrazine
Author(s) -
Magnani M.,
Stocchi V.,
Cucchiarini L.,
Chiarantini L.,
Fornaini G.
Publication year - 1986
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.290040406
Subject(s) - heinz body , phenylhydrazine , hemolysis , phagocytosis , in vivo , red cell , methemoglobin , chemistry , red blood cell , phagolysosome , in vitro , glutathione , biochemistry , hemolytic anemia , haemolysis , lysis , hemoglobin , immunology , biology , enzyme , medicine , macrophage , microbiology and biotechnology , medicinal chemistry
Red blood cells exposed in vitro to phenylhydrazine acquired Heinz bodies, bound autologous IgG and were then phagocytized when incubated with autologus mononuclear phagocytes. In vivo , phenylhdyrazine administered to rabbits, caused the appearance of high plasma hemoglobin levels and hemoglobinuria as well as Heinz body formations and IgG binding to erythrocytes. This suggests that while in vitro the main mechanism of red cell removal seems to be phagocytoses, in vivo both intravascular hemolysis and phagocytosis are active processes. Preliminary biochemical studies on phenylhydrazine‐exposed erythrocytes showed that together with the well‐known appearance of Heinz bodies, methemoglobin and a drop in reduced glutathione, this drug also causes ATP depletion. This is initially concomitant with the appearance of ADP and AMP and subsequently hypoxantine. Thus, irreversible ATP depletion may contribute to the genesis of the hemolytic process observed in vivo .