Hypoxic ischemic encephalopathy (HIE) is one of the main causes of morbidity and mortality during the neonatal period, despite treatment with hypothermia. There is evidence that oxidative
damage plays an important role in the pathophysiology of hypoxic-ischemic (HI) brain injury. Our
aim was to investigate whether postnatal allopurinol administration in combination with hypothermia would reduce oxidative stress (OS) biomarkers in an animal model of HIE. Postnatal 10-day rat
pups underwent unilateral HI of moderate severity. Pups were randomized into: Sham operated,
hypoxic-ischemic (HI), HI + allopurinol (HIA), HI + hypothermia (HIH), and HI + hypothermia
+ allopurinol (HIHA). Biomarkers of OS and antioxidants were evaluated: GSH/GSSG ratio and
carbonyl groups were tested in plasma. Total antioxidant capacity (TAC) was analyzed in plasma and
cerebrospinal fluid, and 8-iso-prostaglandin F2α was measured in brain tissue. Plasma 2,20–azinobis-
(3-ethyl-benzothiazoline-6-sulfonic acid) (ABTS) levels were preserved in those groups that received
allopurinol and dual therapy. In cerebrospinal fluid, only the HIA group presented normal ferric
reducing ability of plasma (FRAP) levels. Protein oxidation and lipid peroxidation were significantly
reduced in all groups treated with hypothermia and allopurinol, thus enhancing neuroprotection
in HIE.
