Aluminium chloride-induced cerebral toxicity in Wistar rats: anticholinesterase and antioxidant effects of ascorbic acid

Numerous literature evidence suggests that aluminium is a toxic metal that induces direct damage to primary human neural cells, leading to genotoxic effects while promoting neurodegeneration in different regions of the brain. However, the use of exogenous antioxidants to counteract neurodegeneration has been widely reported. Ascorbic acid (AA), also known as Vitamin C, is a water-soluble vitamin reported to exert antioxidant, anti-inflammatory and anti-apoptotic effects. Accordingly, this study investigated its protective activity against aluminium chloride (AlCl3)-induced neurotoxicity in Wistar rats. Forty-eight Wistar rats were randomly divided into six groups (n=8) and treated as follows: A (control); B (100 mg/kg bw AlCl3); C (100 mg/Kg bw AA + 100 mg/kg bw AlCl3); D (200 mg/Kg bw AA + 100 mg/kg bw AlCl3); E (100 mg/Kg bw AA); F (100 mg/Kg bw AA). The administration, via an oral gavage, lasted for 28 days. Thereafter, the weights, neurobehavioral, antioxidant enzymes, lipid peroxidation, acetylcholinesterase and histological assessments were carried out. Findings showed significantly (p < 0.05) impaired weights, neurobehavioural, and antioxidant enzymes as well as elevated lipid peroxidation and acetylcholinesterase in the AlCl3-exposed rats when compared to control. Also, the cerebral cortex of AlCl3-exposed rats displayed severe cytoplasmic vacuolations and degenerating cells, indicating cerebral dysfunction. However, pretreatment of AlCl3-exposed rats with AA significantly (p < 0.05) attenuated these adverse effects. Altogether, AA exerted neuroprotective effects against AlCl3-induced cerebral toxicity, possibly through its potent antioxidant and anticholinesterase activity.