Abstract
Significant reduction of methemoglobin to hemoglobin was observed when erythrocytes, previously treated with sufficient sodium nitrite to convert 60-80% of the hemoglobin to methemoglobin, were incubated at 37[degree] C for 3 to 22 hr with certain purine nucleosides (adenosine, aminoadenosine, guanosine, inosine, 2,6-diaminopurine riboside, xanthosine, deoxyadenosine, deoxyguanosine, deoxyinosine), pentoses (ribose, deoxyribose), hexoses (fructose, glucose, galactose), fumaric acid and L (+) sodium lactate. Erythrocytes from a patient with congenital methemoglobinemia were unable to reduce methemoglobin when incubated with compounds that were effective in normal erythrocytes, despite the ability of the congenital methemoglobinemia erythrocytes to produce comparable amounts of lactic acid. Ascorbic acid promoted the reduction of methemoglobin in normal erythrocytes, in hemolysates, and in erythrocytes of congenital methemoglobinemia. Addition of methylene blue to normal erythrocyte suspensions containing added glucose or purine nucleosides accelerated the rate of reduction of methemoglobin and permitted the erythrocytes of congenital methemoglobinemia to reduce methemoglobin in a normal manner. These studies suggest that compounds that can be metabolized by human erythrocytes by pathways that can lead to the reduction of pyridine nucleotides will promote the reduction of methemoglobin, proved the necessary electron transport mechanism is intact.