The effect of asphyxia on iron metabolism and lipid peroxidation in newborn infants with hypoxic–ischemic encephalopathy (HIE) was investigated. Non-protein-bound iron (NPBI) and lipid peroxidation (thiobarbituric-acid-reactive species; TBARS) in plasma and hematological iron indices were measured in 15 healthy newborn infants (mean gestational age 39 04weeks, SD 1); 15 asphyxiated infants without neurological abnormalities (AS–HIE; mean gestational age 38.8 weeks, SD 0.9); and 15 asphyxiated infants with neurological abnormalities (AS+HIE; mean gestational age 39.75 weeks, SD 1.4). Follow-up was performed at the age of 5 months. It was found that the detectable rates of NPBI in 10 of 15 of the AS–HIE group and 13 of 15 of the AS+HIE group were significantly higher than that of the control group (5 of 15; both p<0.01). Plasma levels of TBARS in the control (9.20µmol/L, SD 1.9) and AS–HIE infants (10.13µmol/L, SD 2.7) were significantly lower than those of the AS+HIE group (13.42µmol/L, SD 2.8). Serum iron, total iron binding capacity, and transferrin saturation in the AS+HIE group was higher than the corresponding values of the control and AS–HIE groups, although no statistical difference was found among them. At 5 months of age, all control and AS–HIE infants were neurologically normal, whether or not their NPBI was detectable. Of the 12 AS+HIE infants, four (all of whom had detectable NPBI) were neurologically impaired. The average Gross Development Quotient of AS+HIE infants was significantly lower than that of the control or AS–HIE groups (p<0.01). Results showed that asphyxia could affect iron metabolism and lead to a significant increase in NPBI and lipid peroxidation in newborn infants with HIE, indicating that iron delocalization induced by asphyxia plays a role in the brain injury of asphyxiated infants.