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  • Title: Autocatalytic oxidation of hemoglobin induced by nitrite: activation and chemical inhibition.
    Author: Doyle MP, Herman JG, Dykstra RL.
    Journal: J Free Radic Biol Med; 1985; 1(2):145-53. PubMed ID: 3836241.
    Abstract:
    The nitrite ion is a direct causative agent for methemoglobinemia. Oxidation of hemoglobin to methemoglobin under aerobic conditions is induced by nitrite, catalyzed by methemoglobin in the presence of hydrogen peroxide, and inhibited by chemical reagents ranging from cysteine and ascorbic acid to sulfite. The stoichiometry of nitrate production is dependent on the initial [NO2-]/[HbO2] ratio, but reaches a limiting value of 1:1 [NO3-]: [Hb+] when [NO2-]/[HbO2] greater than 8. Ascorbic acid is an exceptionally effective inhibitor for the autocatalytic oxidation, but its use does not affect the stoichiometry of nitrate formation. Sulfite reduces nitrate production to a level that is half that observed in its absence. These chemical inhibitors act upon the rapid autocatalytic stage for hemoglobin oxidation, but they do not influence the slow direct oxidation of hemoglobin by nitrite. The autocatalytic stage for hemoglobin oxidation results from nitrogen dioxide formed from nitrite through the peroxidase activity of methemoglobin. Peroxide and methemoglobin are formed during the initiation stage by electron transfer from nitrite that is kinetically first order in oxyhemoglobin and in nitrite.
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