Abstract
HEREDITARY methæmoglobinæmia, a rare disorder often associated with a deficiency in NADH-dependent ‘diaphorase’ activity1, has been treated successfully with methylene blue (1–2 mg/kg intravenously) or ascorbic acid (200–500 mg/day orally)2. Methylene blue probably effects the reduction of methæmoglobin by activating the NADPH-dependent methæmoglobin reductase that has been isolated, from human erythrocytes by Kiese et al.3 and by Huennekens et al.4. By serving as electron carriers between NADPH and the methæmoglobin reductase, methylene blue and other artificial electron carriers increase the activity of the hexose monophosphate shunt pathway of glucose metabolism5 and facilitate the reduction of methæmoglobin to hæmoglobin. This NADPH-dependent methæmoglobin reductase system is a reserve mechanism for the reduction of methæmoglobin, for the NADH-dependent ‘diaphorase’ system appears to be the physiologically important pathway in normal human erythrocytes. Ascorbic acid can reduce methæmoglobin to hæmoglobin slowly both in vivo and in vitro, probably through a direct effect on the methæmoglobin2.
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JAFFÉ, E., NEUMANN, G. A Comparison of the Effect of Menadione, Methylene Blue and Ascorbic Acid on the Reduction of Methæmoglobin in vivo. Nature 202, 607–608 (1964). https://doi.org/10.1038/202607a0
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DOI: https://doi.org/10.1038/202607a0
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