Hyperoxic exposure leads to cell death in the developing brain

• Published in: Brain & development (Tokyo. 1979) Vol. 30; no. 9; pp. 556 - 562
• Main Authors: Yiş, Uluç, Kurul, Semra Hız, Kumral, Abdullah, Cilaker, Serap, Tuğyan, Kazım, Genç, Şermin, Yılmaz, Osman
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.10.2008
• Subjects: Animals; Animals, Newborn; Apoptosis; Brain; Brain - cytology; Brain - growth & development; Brain - metabolism; Brain - pathology; Cell Death - physiology; DNA Damage; Female; Humans; Hyperoxia; In Situ Nick-End Labeling; Infant, Newborn; Infant, Premature; Neurology; Neurons - cytology; Neurons - metabolism; Newborn; Organ Size; Oxygen - adverse effects; Pregnancy; Rat; Rats; Rats, Wistar; Brain; Newborn; Rat; Hyperoxia; Apoptosis
• ISSN: 0387-7604; 1872-7131
• DOI: 10.1016/j.braindev.2008.01.010

Abstract Premature infants have high incidence of motor and cognitive impairment in later life. Supraphysiological oxygen concentrations are routinely used in neonatal intensive care units and elicit injury to premature lungs and retina. Since the effects of hyperoxia on the developing brain are scarce, we studied the effects of high oxygen on this tissue. Wistar rat pups were exposed from birth until day 5 to 21% or 80% oxygen. The neuronal density and apoptosis in CA1 and dentate gyrus of hippocampus, prefrontal cortex, parietal cortex, subiculum, and retrosplenial cortex were assessed by immunohistochemistry and ELISA cell death assay. Neuronal density of the investigated brain areas were significantly decreased in the hyperoxia group. Furthermore, using ELISA cell death and TUNEL assays, we observed increased cell death in the developing brain. Our results show that hyperoxia induces cell death in the developing rat brain. This may be one of the important mechanisms that cause motor and cognitive impairment in later life of premature infants.