antioxidants Review How to Improve the Antioxidant Defense in Asphyxiated Newborns—Lessons from Animal Models Hanna Kletkiewicz 1 , Maciej Klimiuk 1, Alina Wo´zniak 2, Celestyna Mila-Kierzenkowska 2 , Karol Dokladny 3 and Justyna Rogalska 1,* 1 Department of Animal Physiology and Neurobiology, Faculty of Biological and Veterinary Sciences, Nicolaus Copernicus University, 87-100 Torun, Poland;
[email protected] (H.K.);
[email protected] (M.K.) 2 Department of Medical Biology and Biochemistry, Faculty of Medicine, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University, 87-100 Torun, Poland;
[email protected] (A.W.);
[email protected] (C.M.-K.) 3 Department of Internal Medicine, School of Medicine, University of New Mexico, Albuquerque, NM 87131, USA;
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[email protected]; Tel.: +48-56-611-26-31 Received: 24 August 2020; Accepted: 15 September 2020; Published: 21 September 2020 Abstract: Oxygen free radicals have been implicated in brain damage after neonatal asphyxia. In the early phase of asphyxia/reoxygenation, changes in antioxidant enzyme activity play a pivotal role in switching on and off the cascade of events that can kill the neurons. Hypoxia/ischemia (H/I) forces the brain to activate endogenous mechanisms (e.g., antioxidant enzymes) to compensate for the lost or broken neural circuits. It is important to evaluate therapies to enhance the self-protective capacity of the brain. In animal models, decreased body temperature during neonatal asphyxia has been shown to increase cerebral antioxidant capacity. However, in preterm or severely asphyxiated newborns this therapy, rather than beneficial seems to be harmful. Thus, seeking new therapeutic approaches to prevent anoxia-induced complications is crucial.