*Dr. Anil Batta


Many illnesses in preterm infants, such as chronic lung disease, necrotizing enterocolitis, retinopathy of prematurity and intracranial hemorrhage, are thought to be related to the action of reactive oxygen species. They occur because the antioxidant system of preterm infants is highly stressed and incompletely developed. Several reports have emphasized the antioxidant role of bilirubin, which in human neonatal plasma seems to have a greater antioxidant capacity than urates, α-tocopherol, or ascorbates. Bilirubin reactions involving free radicals or toxic products of oxygen reduction have been well documented.[2] In particular, unconjugated bilirubin is able to scavenge singlet oxygen with high efficiency, to react with superoxide anions and peroxyl radicals, and to serve as a reducing substrate for peroxidases in the presence of hydrogen peroxide or organic hydroperoxides.[1] However, although the antioxidant effect of bilirubin as a scavenger of reactive oxygen species is well documented in vitroand animal studies, its role in vivo has not been clarified in preterm infants. Yigit et al reported that serum malondialdehyde concentrations were higher in infants with hyperbilirubinemia than in controls and other authors have found a significant correlation between serum bilirubin and total antioxidant capacity of the plasma.[3]

Keywords: Necrotizing enterocolitis, urates, ?-tocopherol or ascorbates.

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