Red blood cell phagocytosis and lysis following oxidative damage by phenylhydrazine.
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.
D004912:Erythrocytes / Q000187:drug effects / Q000276:immunology / Q000502:physiology*; D005455:Fluorescent Antibody Technique; D006801:Humans; D007074:Immunoglobulin G / Q000032:analysis; D009000:Monocytes / Q000502:physiology*; D010084:Oxidation-Reduction; D010587:Phagocytosis; D010659:Phenylhydrazines / Q000494:pharmacology*; D017452:Receptors, IgG; D011971:Receptors, Immunologic / Q000032:analysis
D007074:Immunoglobulin G; D010659:Phenylhydrazines; D017452:Receptors, IgG; D011971:Receptors, Immunologic; C030299:phenylhydrazine