Abstract 228

MnSOD is a powerful antioxidant enzyme that catalyzes disproportionation of O2. Studies have shown that inflammatory cytokines can induce MnSOD production in the liver, thus suggesting a role for MnSOD in the acute phase response. However, whether MnSOD plays a pivotal role in inflammatory processes has not yet been confirmed. Indeed little is known about MnSOD levels in healthy babies and if MnSOD levels would change in response to inflammatory stimuli. In addition, it is not known whether MnSOD levels would correlate with the degree of gestation or change with postnatal age. This study was designed to answer these questions. MnSOD (ELISA) and Mn (mass spectroscopy) levels were measured in 26 neonates (GA:25-40wks) on days 1, 3, and 8 of life and d1 concentrations were correlated with GA; furthermore, we compared MnSOD and Mn levels of neonates who developed IRDS (Gr. 1) with those of infants without pulmonary disease (Gr.2). IRDS was defined as "severe" if FiO2>0.45 and ventilation was required (Gr. 1a); and "mild" if FiO2 ≤040 (Gr1b). In all three groups MnSOD was higher on d1 and decreased with time. MnSOD levels (µM) at all time points were higher in Gr. 1a neonates (243 ± 164, 213 ± 171; and 142±110) than in Gr.2 (164±261, 125±71, and 52±36), however, statistically significant differences (Student t-test) were reached on d8 only. Mn levels (ng/mL) in these two groups were 4±2, 6±4, 4±1 (Gr. 1a), and 7±4, 6±4, 4±2 (Gr.2). No differences in Mn or MnSOD levels were observed between Gr. 1b and neither Gr. 1a nor Gr.2. In neonates without lung disease, d1 MnSOD inversely correlated(Pearson) with GA (r=-0.853, p=0.015). We conclude that MnSOD is high in the plasma of preterm infants and likely participates in the inflammatory response occurring during IRDS.