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Observations on the Mechanism of Action of Acetylphenyl‐hydrazine in Normal and Glucose‐6‐Phosphate Dehydrogenase (G‐6‐PD) Deficient Erythrocytes
Author(s) -
Stuart Gary A.
Publication year - 1969
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1969.tb00421.x
Subject(s) - chemistry , mechanism of action , glutathione , red cell , incubation , red blood cell , glucose 6 phosphate dehydrogenase , biochemistry , hydrazine (antidepressant) , dehydrogenase , biophysics , enzyme , medicine , in vitro , biology
Summary: Evidence is presented that two mechanisms of action account for the GSH instability of G6‐PD‐deficient erythrocytes following incubation with acetylphenylhydrazine. In Mechanism A, also manifested by the normal cell, acetylphenylhydrazine has the characteristics of an inhibitor which stoicheiometrically prevents the maintenance of an amount of GSH proportional to the dose of the drug. In Mechanism B the effect of acetylphenylhydrazine is proportional to the red cell concentration indicating an excess of the drug relative to its site of action. The loss of GSH by both mechanisms is related to the severity of the G‐6‐PD deficiency. Additional experiments show that mechanisms of action similar to those exhibited by the G6‐PD‐deficient erythrocyte exist in the normal red cell suspended in a galactose solution or in solutions containing low quantities of glucose.