Abstract
Summary
Cobaltous chloride in concentrations up to 8.0 mM in human red cell suspensions in a Krebs-Ringer-bicarbonate-glucose media produced significant hemolysis under O2 but not under N2. Both O2 and cobalt have significant hemolytic effects and appear to greatly potentiate each other. Hemolysis favors methemoglobin accumulation in the extracellular fluid, but O2 has an additional effect in the opposite direction. By keeping the hemoglobin saturated, oxygen tends to prevent auto-oxidation of the pigment to methemoglobin. Thus, methemoglobin accumulation in erythrocyte suspensions exposed to cobalt is a net result of several opposing effects, but no evidence was obtained to suggest that cobalt is a specific inhibitor of methemoglobin reductase.
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