EFFECT OF MANNITOL AND URIC ACID ON LIPID PEROXIDATION AND LEVEL OF CREATINE KINASE IN ALBINO RATS INDUCED WITH TRAUMATIC BRAIN INJURY
Suleiman N., *Bulama I., Suleiman M., Bilbis L. S. and Saidu Y.
Traumatic brain injury causes massive production of reactive oxygen species with resultant oxidative stress and impairment of endogenous antioxidant defense mechanisms. This study investigated the role of antioxidants in the management of traumatic brain injury. Truamatic brain injury was induced in 30 randomly selected winstar rats using weight drop method. The rats were divided into 6 groups of 5 rats each. Groups 1 & 2 were treated with 22.5mg/kg and 45mg/kg of mannitol while 3 & 4 were treated with same doses of uric acid orally for 14 days. Neurological assessment was done using Modified Glasgow coma scale. Blood and brain tissues were collected and analysis on lipid peroxidation and level of creatine kinase was conducted. The results showed that TBI significantly increased (P<0.05) malondialdehyde concentration and creatine kinase activity. Supplementation with the antioxidants however reversed the trend in a dose dependent manner and decreased the mortality. In conclusion supplementation with mannitol and uric acid might have replenished the antioxidant defense system and have reduced oxidative lipid damage and therefore oxidative stress that is associated with increased mortality in TBI. This study highlighted the potentials for the use of antioxidants in the management of TBI.
Keywords: Oxidative stress, Antioxidant, Glasgow coma scale.
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