| Abstrakt: |
Background: The brain is highly susceptible to Aluminium’s (Al) toxic impact due to its elevated lipid content and oxygen utilization but, relatively scanty levels of antioxidants. Al is known for its strong pro-oxidant activity. Hence oxidative stress in the brain is a likely outcome of Al toxicity. Previous studies report sensory, motor and cognitive deficits in animals exposed to various Al compounds. Hence, this study was undertaken to find how dose, and time span of aluminium exposure influence the pro-oxidant activity and antioxidant handling capacity in female Wistar rats’ cerebellum and hippocampus. Materials and Methods: Two groups of female Wistar rats were given four different aluminium chloride oral doses of 0, 50, 100, 200 mg/Kg body weight daily for a time span of four and eight weeks. Oxidative level was assessed by estimating GSH, LPO, SOD, Catalase, GPx and GR in cerebellum and hippocampus of rat brain. Data was analysed by 2-way ANOVA and Bonferroni ‘t’ test was used for multiple group comparisons. Results: Al exposure in female rats resulted in increased lipid peroxidation, while antioxidants GSH, SOD, catalase, GPx and GR were depleted in cerebellum and hippocampus. However, these changes were predominantly significant only in aluminium doses of 100 and 200 mg/Kg in both 4 and 8weeks studies. But, GPx in the cerebellum and catalase in hippocampus showed a crucial reduction even at 50 mg/Kg dose on eight-week exposure. Conclusion: Aluminium has enhanced the synthesis of Reactive Oxygen Species (ROS) in rat cerebellum and hippocampus, as noted by the increase in lipid peroxidation which was not balanced by the elevated synthesis of antioxidants. In addition, aluminium at higher doses of 100mg/Kg dose and more had a significant negative impact on the antioxidant protective system. Therefore, it is vital to minimize our aluminium exposure from different sources in our everyday lives. [ABSTRACT FROM AUTHOR] |
