Deficient activity of DPNH-dependent methemoglobin diaphorase in cord blood erythrocytes.

Y OUNG INFANTS are unusually susceptible to the development of methemoglobinemia upon exposure to certain medications and toxic agents. Ingestion of well water containing large quantities of nitrate will cause methemoglobinemia in small babies while older members of the family remain unaffected.14 Bismuth subnitrate, benzocaine, resorcin or aniline dye, taken by mouth or absorbed rectally or percutaneously, will produce severe methemoglobinemia in infants in amounts which cause no abnormality in older individuals.513 Previous work indicated that umbilical cord blood erythrocytes exhibit a diminished ability to reduce methemoglobin in vitro in the presence of substrate capable of generating reduced diphosphopyridine nucleotide ( DPNH ). From this it was postulated that the defect was due either to a transient neonatal deficiency of DPNH-dependent methemoglobin reductase, or diaphorase, or to inadequate generation of the DPNH necessary for the action of this enzyme.14 The present study was undertaken to determine whether there is a deficiency of methemoglobin diaphorasef in cord blood erythrocytes. Persistence of such a defect through the first weeks or months of life could explain the increased tendency to acquired methemoglobinemia in this age group.