97 ELECTRON PARAMAGNETIC RESONANCE (EPR) MONITORING OF ASCURBATE FREE RADICAL (A*) AS MARKER OF INCREASED IRON-MEDIATED OXIDATIVE DAMAGE (MOD) IN PLASMA OF NEONTES

In common neonatal disorders (hemolytic disease, asphyxia, hypoperfusion) as well as in red cell transfusion the oxidative risk can increase, as free iron is released from damaged tissues and promotes conversion of hydroperoxides into the highly reactive hydroxyl/alkoxyl radicals. In this reaction ascorbate is concurrently oxidized to A-. To investigate the capability of neonatal plasma to counteract IMOD, samples of pre-term (11 subjects, GA 28-35 wks) and term infants (11 normals, GA 38-42 wks) were challenged with scalar amounts of Fe++, as well as plasma of 7 adult controls. The reaction was evaluated by EPR monitoring of the A-produced.RESULTS: 1) althought A-production was slighly lower than in adults, the Fe++µM which triggered the reaction were significantly smaller in pre-term and term infants (21.1 ± 6.0 and 31.1 ± 10.3 vs. 43.7 ± 4.6; P<0.001 and < 0.05). This difference was not referable to a different saturation of transferrin since the total and latent iron binding capacity of plasma was similar both in neonatal and adult samples. 2) in contrast with adults, in pre-term and term infants (P<0.001) the EPR segnal persisted for a longer time and after 15 min. A-values were still 69.2 ± 8.9 and 63.5 ± 23.3 per cent of initial peak. CONCLUSIONS: 1) Neonates have a reduced tolerance to IMOD; 2) In this condition ascorbate behaves as a pro-oxidant, instead of antioxidant compound and its administration can be dangerous; 3) Prevention of IMOD should be directed to the search for effective iron chelators.