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May 18, 2022Keywords:
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Main Article Content
Ascorbic acid modulates prefrontal cortex cellular changes in androgen deprived rats
Abstract
Background: Testosterone deficiency has been implicated in numerous neurodegenerative diseases such as Alzheimer's, Parkinson and Huntington's disease. We used a model of androgen deprived rats to determine the effects of ascorbic acid on prefrontal cortex (PFC) cellular changes associated with a subset population of androgen deprived patients.
Methodology: Chemical castration (using testosterone antagonist) as well as orchiectomy can induce androgen deprivation. Twenty-one (21) adult male Wistar rats with an average weight of 170g±10g were randomly assigned into three groups with each group containing seven (7) rats. Group A was control group, Group B= Orchiectomy + Flutamide (11 mg/kg body weight), and group C= Orchiectomy + Flutamide (11 mg/kg body weight)+Ascorbic acid (100 mg/kg body weight). Treatment lasted for 30 days. Nitric oxide and Malondialdehyde levels were assessed; while serum testosterone level was assayed. Histological, Histochemical, and immunohistochemical investigations were performed using Hematoxylin & Eosin, Cresyl fast violet, and Bielschowsky stains respectively.
Result: Our results showed increased expression of Nitric Oxide (NO), and increased lipid peroxidation (MDA) in the PFC of orchiectomized animals with altered cytoarchitectural morphology evidenced by decreased Nissl staining polarity in neuronal axons and aggregation of neurofibrillary tangles. Oxidative and nitrosative stress were well modulated in animals treated with ascorbic acid with unaltered prefrontal cortex morphology.
Conclusion: The results indicated that decline in brain androgen activities caused nitrosative and oxidative stress-driven pathology in the prefrontal cortex while supplementing endogenous ascorbic acid offered therapeutic value by scavenging free radicals in the prefrontal cortex
