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  • 1
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochemical and Biophysical Research Communications 125 (1984), S. 14-17 
    ISSN: 0006-291X
    Keywords: [abr] G6PD; glucose 6-phosphate dehydrogenase ; [abr] HMP; hexose monophosphate pathway ; [abr] Hb; hemoglobin ; [abr] RBC; Red blood cells
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 2
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochemical and Biophysical Research Communications 125 (1984), S. 14-17 
    ISSN: 0006-291X
    Keywords: [abr] G6PD; glucose 6-phosphate dehydrogenase ; [abr] HMP; hexose monophosphate pathway ; [abr] Hb; hemoglobin ; [abr] RBC; Red blood cells
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 3
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    Cell Biochemistry and Function 4 (1986), S. 263-269 
    ISSN: 0263-6484
    Keywords: Erythrocytes ; IgG-binding ; oxidative hemolysis ; phenylhydrazine ; Chemistry ; Biochemistry and Biotechnology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: 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.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    Cell Biochemistry and Function 6 (1988), S. 175-182 
    ISSN: 0263-6484
    Keywords: Erythrocytes ; glucose metabolism ; uncleotide catabolism ; phenylhydrazine ; Chemistry ; Biochemistry and Biotechnology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: In addition to the well known effect of phenylhydrazine on red blood cells (methaemoglobin and Heinz body formation, autologous IgG binding, lipid peroxidation, etc.) an increased glucose utilization was observed. Measurement of 14CO2 formation from [1-14C]-glucose showed a maximum value at 2 mM phenylhydrazine followed by a progressive inhibition on increasing the drug concentration to 16 mM. Concomitantly we found a reduction in the reduced glutathione concentration but not a corresponding increase in the level of oxidized glutathione. Phenylhydrazine also causes ATP depletion. The ATP is in part dephosphorylated to ADP and AMP and in part converted to inosine monophosphate and hypoxanthine. Measurement of the cell content of reduced and oxidized pyridine nucleotides was also performed and showed a progressive increase in the reduced forms of these coenzymes. Thus phenylhydrazine promotes cellular ATP depletion followed by adenine nucleotide catabolism that is not efficiently counteracted by an increase in glucose utilization. The relevance of these data to the mechanism of phenylhydrazine-induced anemia is discussed.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
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