RESUMO
The role of selenium in man is diverse. In particular, selenium is a cofactor of the major antioxidative enzyme glutathione peroxidase, which inhibits free radical oxidation reactions and restores the normal vital functions of cells and organs. This study deals with selenium metabolism in severe brain injury and its correction modes.
Assuntos
Antioxidantes/metabolismo , Traumatismos Craniocerebrais , Eritrócitos/metabolismo , Traumatismo Múltiplo , Selênio , Criança , Traumatismos Craniocerebrais/sangue , Traumatismos Craniocerebrais/metabolismo , Traumatismos Craniocerebrais/urina , Feminino , Humanos , Cinética , Peroxidação de Lipídeos , Masculino , Traumatismo Múltiplo/sangue , Traumatismo Múltiplo/metabolismo , Traumatismo Múltiplo/urina , Selênio/sangue , Selênio/metabolismo , Selênio/urina , Índice de Gravidade de DoençaRESUMO
Changes in the products of lipid peroxidation (LPO) and the antioxidative system (AOS) were studied in 94 children aged 3 to 15 years with severe brain injury (BI) on days 1, 3-5, and 7-10. The contents of dienic conjugates and malonic dialdehyde and the level of induced peroxide hemolysis and peroxide resistance of red blood cells in the plasma were determined. Children with severe BI were found to have activated LPO processes and decreased AOS activity, the most significant changes occurring within 24 hours of injury. The increased activity of peroxide processes was attended by reverse AOS changes. In children, the time course of changes in the parameters of LPO and AOS differs from that in adults since there is no phase of excessive LPO activation due to the exhaustion of AOS reserves.
