Abstract
Aluminium is known to accelerate oxidative stress, amyloid beta (Aβ) deposition, and plaque formation in the brain of rats. Objective. The present study is aimed at studying the neuroprotective effects of eugenol following aluminium-induced neurotoxicity on caspase-3, apoptotic proteins (Bcl-2 and Bax), and oxidative stress markers in Wistar rats such as superoxide dismutase (SOD), glutathione peroxidase (GPx), nitric oxide (NO), and assay oxidative stress to mitochondrial DNA (mtDNA) by measuring the levels of 8-hydroxy-2-deoxyguanosine (8-OHdG). Materials and methods. Twenty (20) adult Wistar rats were randomly divided into four (4) groups with five animals in each group. Route of administration was oral throughout the duration of this study and this study lasted for 21 days. Rats were sacrificed 24 hours after administration of the last dose (i.e., day 22) with 0.8 mg/kg ketamine as an anaesthetic agent. Results. Exposure to AlCl3 resulted in a significant (p < 0.01) elevation in the levels of nitric oxide and 8-hydroxy-2-deoxyguanosine (8-OHdG), enhanced the activity of caspase-3, increased the level of proapoptotic protein Bax and reduced the levels of antiapoptotic protein Bcl-2, and significantly (p < 0.01) reduced the levels of SOD and GPx. However, treatment with eugenol resulted in a significant reduction (p < 0.01) in the levels of nitric oxide (NO) and 8-hydroxy-2-deoxyguanosine (8-OHdG) levels, inhibited the activity of caspase-3, increased levels of Bcl-2 and significantly (p < 0.05) reduced levels of Bax protein, respectively, and also significantly (p < 0.05) increased the levels of SOD and GPx. Our results would hereby suggest that eugenol would provide a therapeutic value against aluminium-induced oxidative stress as related to antioxidant and antiapoptotic activities.
Highlights
IntroductionAluminium (Al) is ever present in our environment
The present study revealed an increase in nitric oxide production as shown in Figure 4, indicating that aluminiuminduced toxicity can result in changes in nitric oxide generation [31]
Exposure to aluminium chloride can result in the generation of free radicals, which resulted in the elevation of nitric oxide levels and reduction in the enzymatic and nonenzymatic antioxidant components
Summary
Aluminium (Al) is ever present in our environment. Food is the major source for aluminium intake under physiological conditions [1]. The widespread presence of aluminium, both in the environment and in food, makes it almost impossible to avoid exposure to this metal ion [2]. Aluminium appears to react with the superoxide radical, facilitating its destructive potential [3]. Experimental observations indicate that formation of the superoxide plays a major step in contributing to excitotoxicity-mediated neuronal death through generation or production of peroxynitrite [4]. Aluminium could enhance excitotoxicity by inducing apoptosis of astrocyte. Astrocytes are thought to be a primary target of aluminium accumulation among neuronal
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