ABSTRACT
The oxygen-detoxifying enzymes of neutrophils, SOD, GPX, and catalase, were measured in neutrophils obtained from normal human infants, their mothers, and controls to determine whether or not the impaired functions of infant neutrophils might be related to a decreased ability of these cells to detoxify reactive forms of oxygen. The rationale was based on the following. (1) Defective functions have been reported in neutrophils sustaining oxidative damage. (2) Increased oxidative metabolism and decreased functions can be demonstrated concomitantly in infant neutrophils. (3) Neutrophils from infants may be analogous to infant erythrocytes, cells known to exhibit increased susceptibility to oxidative injury and dysfunctions that are apparently related to deficiencies of GPX and catalase. SOD activity was similar in neutrophils obtained from infants, their mothers, and controls, whereas both GPX and catalase were significantly decreased in infant cells. The data suggest that infant neutrophils were rendered susceptible to oxidative damage and possibly to defective function by an imbalance of oxygen-detoxifying enzymes.
Subject(s)
Glutathione Peroxidase/metabolism , Neutrophils/enzymology , Oxygen/metabolism , Peroxidases/metabolism , Superoxide Dismutase/metabolism , Superoxides/metabolism , Adult , Female , Humans , Infant, Newborn , Neutrophils/metabolismABSTRACT
Postphagocytic chemiluminescence of neutrophils was evaluated in infants throughout the 1st month of life, in their mothers and healthy adults to investigate further the defective chemiluminescence of neonatal neutrophils described by earlier studies. Maternal and adult values were similar and served as controls. Abnormalities both of peak chemiluminescence and of the kinetics of light emission were detected in infant neutrophils throughout the 1st month of life. Infant responses were variable, particularly at birth, when neutrophils of some infants performed comparably to those of controls.
