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Experimental neonatal hypoxia ischemia causes long lasting changes of oxidative stress parameters in the hippocampus
Felipe Kawa Odorcyk1, Janaína Kolling2, Eduardo Farias Sanches3
1Post-graduation Program of Neurosciences, Departamento de Bioquímica, Instituto das Ciências da Saúde (ICBS), Universidade Federal do Rio Grande do Sul, Rua Ramiro Barcelos, 2600 anexo 90035-003, Porto Alegre, RS, Brazil, Tel./Fax: 0055-051 33085568.
Abstract:
Neonatal hypoxia ischemia (HI) is the main cause of mortality and morbidity in newborns. The mechanisms involved in its progression start immediately and persist for several days. Oxidative stress and inflammation are determinant factors of the severity of the final lesion. The spleen plays a major part in the inflammatory response to HI. This study assessed the temporal progression of HI-induced alterations in oxidative stress parameters in the hippocampus, the most affected brain structure, and in the spleen. HI was induced in Wistar rat pups in post-natal day 7. Production of reactive oxygen species (ROS), and the activity of the anti oxidant enzyme superoxide dismutase and catalase were assessed 24 h, 96 h and 38 days post-HI. Interestingly, both structures showed a similar pattern, with few alterations in the production of ROS species up to 96 h often combined with an increased activity of the anti oxidant enzymes. However, 38 days after the injury, ROS were at the highest in both structures, coupled with a decrease in the activity of the enzymes. Altogether, present results suggest that HI causes long lasting alterations in the hippocampus as well as in the spleen, suggesting a possible target for delayed treatments for HI.
