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Utilization of red‐cell FAD by methaemoglobin reductases at the expense of glutathione reductase in heterozygous β ‐thalassaemia
Author(s) -
Perry G. M.,
Anderson B. B.
Publication year - 1991
Publication title -
european journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0902-4441
DOI - 10.1111/j.1600-0609.1991.tb01541.x
Subject(s) - glutathione reductase , red cell , glutathione , reductase , methemoglobin , oxidative stress , heterozygote advantage , medicine , endocrinology , chemistry , biochemistry , biology , enzyme , hemoglobin , glutathione peroxidase , allele , gene
FAD‐dependent methaemoglobin reductases (MHR) were studied in red cells in heterozygous β‐thalassaemia to investigate how they related to low FAD‐dependent glutathione reductase (GR). In contrast to GR, MHR activities were usually normal or increased. In particular, whether expressed in relation to haemoglobin or number of red cells, NADPH‐MHR activity was markedly increased in most subjects, probably being a response to increased oxidative stress. Oral riboflavin had no effect on MHR activities, indicating saturation with FAD even though GR was deficient. A strong correlation between percent stimulation of GR by FAD and NAPDH‐MHR activity indicates that FAD is utilized by MHR at the expense of GR. This could be an important influence on GR in heterozygous β‐thalassaemia. Thus, the low activity resulting from an inherited deficiency of FAD is decreased further.