Effect of some low molecular mass antioxidants in the management of traumatic Brain injury in albino rats

Excessive generation of reactive oxygen species (ROS) and impairment of endogenous antioxidant defense mechanism begins immediately after traumatic brain injury (TBI), resulting in secondary events leading to neuronal dysfunction and death. This study reports the role of some low molecular mass antioxidantsin the management of TBI. Winstar rats subjected to closed head injury using an accelerated impact device were administered 22.5mg/kg and 45mg/kg body weight of some of the low molecular mass antioxidants (LMMA) for two weeks. Modified Glasgow coma scale (MGCS) was performed to ascertain the level of consciousness. Blood and brain tissues were collected and analyzed for oxidative stress biomarkers and histological appearances respectively. The results indicated that TBI caused significant decrease (P<0.05) superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities, and significantly increase (P<0.05) malondialdehyde (MDA) concentration. Supplementation with some LMMA however reverted the trend and decreased the healing time and mortality. Histology also showed interparanchymal hemorrhage in traumatized-non-treated rats group, and healing/normal brain sections in the TBI antioxidants supplemented groups. Supplementation of antioxidants to TBI induced rats reduced the impact of oxidative stress and may be responsible for the observed reduction in mortality rate and healing time in the traumatised rats.