THE work of Beutler1 on erythrocyte glutathione ‘instability’ has demonstrated the significance of the glutathione content of red cells for the maintenance of overall erythrocyte structure (and presumably function). In addition, Rigas et al.2 have shown how the interaction of haemoglobin and oxidized glutathione can lead to increased rates of splenic erythrocyte destruction. A number of disease states have been related to increased instability of erythrocyte glutathione; for example, Theil et al.3 have shown a significant decrease of blood glutathione-levels in patients with acute renal insufficiency.
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