Reaktif Oksigen Spesies pada Cedera Otak Traumatik

Abstract Traumatic Brain Injury (TBI) morbidity and mortality are due to primary and secondary injury. Primary injury is due to mechanical forces during the trauma process and secondary injury is subsequent process following the primary impact. This secondary injury processes involving increased excitatory amino acids, ionic imbalance, decreased ATP level, unusual proteolytic enzyme activity, and oxidative stress which contibute to delayed neuronal dysfunction and neuronal death. The mammalian brain is vulnerable to oxidative stress because of the high oxygen consumption needed for maintaining neuronal ion homoeostasis during the propagation of action potentials.There is a close relationship between degree of oxidative stress and severity of brain insults, which results from a perturbation of calcium homeostasis, energy metabolism, and increased lipid peroxidation. In this review we discuss oxidative stress during traumatic brain injury, and it’s implication on pathology of traumatic brain injury.