Abstract
To account for impaired bactericidal activity of polymorphonuclear leukocytes during galactosemia, we have investigated the effects of galactose upon free radical reactions associated with the oxygen-dependent killing mechanism of guinea pig polymorphonuclear leukocytes. Millimolar levels of galactose, which are encountered in the circulation of infants with galactosemia, did not affect the chemical reaction of Superoxide anion with either ferricytochrome c or nitroblue tetrazolium. Galactose did, however, significantly inhibit the reaction of hydroxyl radical with methional, and we propose that such hydroxyl radical removal would be deleterious to normal bactericidal activity. Additional experiments demonstrated that polymorphonuclear leukocytes incubated in the presence of galactose reduced less ferricytochrome c than polymorphonuclear leukocytes incubated without galactose. These results imply that galactose impairs the cellular release of Superoxide anion, which would further disable bactericidal activity.
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