The combined effects of zinc oxide nanoparticles (ZnONP) and ascorbic acid (AA) in the regulation of aluminum (Al) induced rat model of Alzheimer’s disease (AD)-like dementia were investigated with a focus on oxidative stress regulation and long term memory functions. Spraque Dawley rats were grouped as: Control; Al; Al + ZnONP + AA; ZnONP + AA. AlCl3 (70 mg/kg/d) was administered i.p. for 42 days. Starting from day 14, ZnONP (1 mg/kg) and AA (125 mg/kg) were administered i.p. for 28 days. Passive avoidance test was performed and hyperphosphorylated tau (p-tau) was quantified by indirect immunofluorescence. Acetylcholine esterase (AChE) activity was measured for synaptic transmission control. Levels of endogenous antioxidants (superoxide dismutase, catalase, total glutathione), lipid peroxidation and total antioxidant capacity (TAC) were determined. Light microscopic histological changes of the brain prefrontal cortex were evaluated. Neuronal DNA damage was determined by the comet assay. Significant passive avoidance memory impairment was accompanied by the strong AChE activation, p-tau accumulation, high level of oxidative stress, DNA damage and histopathological changes of the brain in Al group of animals. ZnONP-AA co-administration improved passive avoidance dysfunction, normalized AChE activity and p-tau. Neuronal DNA damage was significantly decreased and histology of the brain was maintained. ZnONP-AA co-administration supported TAC of the brain in Al-induced rats and also regulated endogenous antoxidants leading to a significant decrease in OS and AD-like pathology. Consequently, long-term memory functions were significantly improved.
Uçarcan et al. (Sun,) studied this question.