Hypothermia can reverse hepatic oxidative stress damage induced by hypoxia in rats

• Manuel Vicente Garnacho-Castaño ^[1] ; Norma Alva ^[2] ; Sergio Sánchez-Nuño ^[2] ; Raquel G. Bardallo ^[2] ; Jesús Palomeque ^[2] ; Teresa Carbonell ^[2]
  1. [1] Universitat Pompeu Fabra

     Universitat Pompeu Fabra

     Barcelona, España

     
  2. [2] Universitat de Barcelona

     Universitat de Barcelona

     Barcelona, España

     
• Localización: Journal of physiology and biochemistry, ISSN-e 1877-8755, ISSN 1138-7548, Vol. 72, Nº. 4, 2016, págs. 615-623
• Idioma: inglés
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• Resumen

  • Our previous findings demonstrated that hypothermia enhances the reduction potential in the liver and helps to maintain the plasmatic antioxidant pool. Here, we aimed to elucidate if hypothermia protects against hypoxia-induced oxidative stress damage in rat liver. Several hepatic markers of oxidative stress were compared in three groups of animals (n = 8 in each group): control normothermic group ventilated with room air and two groups under extreme hypoxia (breathing 10 % O2), one kept at normothermia (HN) (37 °C) and the other under deep hypothermia (HH) (central body temperature of 21–22 °C). Hypoxia in normothermia significantly increased the levels of hepatic nitric oxide, inducible nitric oxide synthase expression, protein oxidation, Carbonilated proteins, advanced oxidation protein products, 4-hydroxynonenal (HNE) protein adducts, and lipid peroxidation when compared to the control group (p < 0.05). However, when hypoxia was induced under hypothermia, results from the oxidative stress biomarker analyses did not differ significantly from those found in the control group. Indeed, 4-HNE protein adduct amounts were significantly lower in the HH versus HN group (p < 0.05). Therefore, hypothermia can mitigate hypoxia-induced oxidative stress damage in rat liver. These effects could help clarify the mechanisms of action of therapeutic hypothermia.