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<mods:namePart>Durán Fernández-Feijóo, Cristina</mods:namePart>
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<mods:namePart>Rodríguez-Fanjul, Javier</mods:namePart>
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<mods:namePart>López-Abat, Miriam</mods:namePart>
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<mods:namePart>Cavia Saiz, Mónica</mods:namePart>
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<mods:namePart>Muñiz Rodríguez, Pilar</mods:namePart>
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<mods:namePart>Arnaez, Juan</mods:namePart>
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<mods:namePart>Fernández-Lorenzo, José Ramón</mods:namePart>
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<mods:namePart>Camprubí Camprubí, Marta</mods:namePart>
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<mods:identifier type="uri">http://hdl.handle.net/10259/8069</mods:identifier>
<mods:identifier type="doi">10.3390/antiox10101523</mods:identifier>
<mods:identifier type="essn">2076-3921</mods:identifier>
<mods:abstract>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&#xd;
damage plays an important role in the pathophysiology of hypoxic-ischemic (HI) brain injury. Our&#xd;
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&#xd;
pups underwent unilateral HI of moderate severity. Pups were randomized into: Sham operated,&#xd;
hypoxic-ischemic (HI), HI + allopurinol (HIA), HI + hypothermia (HIH), and HI + hypothermia&#xd;
+ allopurinol (HIHA). Biomarkers of OS and antioxidants were evaluated: GSH/GSSG ratio and&#xd;
carbonyl groups were tested in plasma. Total antioxidant capacity (TAC) was analyzed in plasma and&#xd;
cerebrospinal fluid, and 8-iso-prostaglandin F2α was measured in brain tissue. Plasma 2,20–azinobis-&#xd;
(3-ethyl-benzothiazoline-6-sulfonic acid) (ABTS) levels were preserved in those groups that received&#xd;
allopurinol and dual therapy. In cerebrospinal fluid, only the HIA group presented normal ferric&#xd;
reducing ability of plasma (FRAP) levels. Protein oxidation and lipid peroxidation were significantly&#xd;
reduced in all groups treated with hypothermia and allopurinol, thus enhancing neuroprotection&#xd;
in HIE.</mods:abstract>
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<mods:languageTerm authority="rfc3066">eng</mods:languageTerm>
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<mods:accessCondition type="useAndReproduction">Atribución 4.0 Internacional</mods:accessCondition>
<mods:subject>
<mods:topic>Allopurinol</mods:topic>
</mods:subject>
<mods:subject>
<mods:topic>Hypothermia</mods:topic>
</mods:subject>
<mods:subject>
<mods:topic>Hypoxic-ischemic encephalopathy</mods:topic>
</mods:subject>
<mods:subject>
<mods:topic>Oxidative stress</mods:topic>
</mods:subject>
<mods:subject>
<mods:topic>Oxidative damage</mods:topic>
</mods:subject>
<mods:titleInfo>
<mods:title>Effects of Hypothermia and Allopurinol on Oxidative Status in a Rat Model of Hypoxic Ischemic Encephalopathy</mods:title>
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