Abstract
Beutler and Mathai1 have rather simplified my thesis2. A central theme, that the methaemoglobin–oxyhaemoglobin and oxidized-reduced glutathione (GSSG–GSH) systems are loosely linked in a buffering system against the selective and destructive effects of different types of oxidizing compound, has already been discussed3. On the basis of published4–10 and otherwise unpublished2 observations, it was also proposed that the pentose phosphate pathway governs the equilibrium between methaemoglobin formation and GSH depletion, and thus generally between the degrees of methaemoglobinaemia and haemolysis in eryfchrocytes exposed to catalytic oxidants. The suggestion was made that, by providing a source of reductant energy which varies in degree and direction with the oxidant stress, the pentose phosphate pathway might well have played an important part in the evolution of the anuclear mammalian erythrocyte. These concepts, relating to the adaptive role of the pentose phosphate pathway, seemed essentially in accord with previous and concurrent observations concerning the role and control of the pentose phosphate pathway in other mammalian tissues (see refs. 11–22, and refs. 70–74 cited by Jandl et al.23
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HARLEY, J. Significance and Regulation of Methaemoglobinaemia. Nature 210, 1164 (1966). https://doi.org/10.1038/2101164a0
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DOI: https://doi.org/10.1038/2101164a0
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