The mode of action of the nitrite ion on intact human erythrocytes has been investigated under varying experimental conditions. Nitrite appeared to act directly to cause methemoglobin formation and GSH depletion. Evidence was presented to show that such depletion does not occur in the presence of a normal and active pentose phosphate pathway, and to suggest that methemoglobin formation buffers the erythrocyte against nitrite-induced oxidation of GSH.

Both in the presence and absence of glucose, nitrite in high concentration was found to cause increased rates of oxidative destruction of hemoglobin with Heinz body formation, and of loss of osmotic integrity. It was suggested that nitrite acts by "simple" oxidation of the -SH groups of globin and other erythrocytic components, and possibly by causing deamination of cellular proteins.

The results were discussed, with reference to the significance of cellular protective mechanisms under evolutionary or environmental conditions which involve intermittent exposure to high concentrations of the nitrite ion.

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