Immature birth exposes the neonate to conditions of hyperoxia compared to intrauterine environment. Antioxidant defense mechanisms are inadequate to handle an increase in oxygen radicals. Furthermore inadequate antioxidant defense is implicated in the pathophysiology of bronchopulmonary dysplasia, retinopathy, necrotizing enterocolitis or intraventricular hemorrhage.

It has been shown that Glutathion-S-transferase (GST) activity in red blood cells is a usefull indicator of oxidative stress in adults. The iso-enzym of GST most abundant in erythrocytes is inactivated by oxidative stress and it is not replaced.

Objective: Using GST as a marker we tested a)whether birth is an oxidative stress and b)whether sick premature infants are exposed to more oxidative stress than healthy ones.

Patients: 40 infants with gestational age ranging from 24 to 34 weeks were included. Eleven infants (11/40)required intensive care in the first week of life due to IRDS, sepsis, cardiovascular instability.

Methods: GST was measured in erythrocytes using GST-activity towards 1-chloro-2,4-dinitrobenzene. Samples were taken from umbilical cord blood, and at 3, 24 and 48 hs postpartum. Not all patients had four samples.

Results: There was a significant decrease of GST at 3 hours postpartum compared to GST in umbilical cord blood.(p<0.01, n=15, ANOVA). Furthermore, GST activity in red cells of sick premature infants showed a significant decrease in the first 48 hours (p< 0.01, ANOVA), whereas GST activity in erythrocytes of healthy infants did not show a significant decrease. (see table below)

Table 1
Full size table

GST activity U/gHb (mean + SD) in red cells of premature infants in cord blood and at 3, 24, 48 hours postpartum.

Conclusions: Birth and severe disease are an oxidative stress to the prematurely born infant.