Regenerative and Anti-inflammatory Roles of Ascorbic Acid in Alcohol-Induced Neuroendocrine Degeneration

Abstract

Chronic alcohol consumption is a major cause of metabolic dysfunction and neurodegeneration, yet therapeutic strategies remain limited. Excessive production of free radicals is capable of causing oxidative destruction to biomolecules (lipids, proteins, and DNA), eventually resulting in long-term conditions like stroke, aging, and other neurological illnesses. Hence, the purpose of this study is to look into the possible effect of alcohol abuse to capture chronic toxicity, while co-administered vitamin C at an effective antioxidant dose assesses its potential to mitigate alcohol-induced oxidative damage and neurodegeneration. A total of twenty male rabbits were randomized into four groups: control (A), alcohol only (B), alcohol + vitamin C (C), and alcohol + vitamin C with a recovery period (D). Alcohol administration involved 2 ml of 20% alcohol daily for 30 days, escalating to 4 ml for 24 days, totaling 54 days. Body weight and blood glucose were monitored, and histological analyses of the cerebrum and cerebellum were performed post-treatment. Results showed that alcohol-treated groups exhibited significant hyperglycemia and marked histopathological alterations, including neuronal shrinkage, vacuolation, and reactive gliosis in both cerebrum and cerebellum. Ascorbic acid supplementation partially attenuated these effects but did not fully restore normal histoarchitecture or glucose homeostasis. Recovery periods without alcohol reduced but did not eliminate neurodegenerative changes. In conclusion, prolonged alcohol exposure induces persistent metabolic and neurodegenerative changes, while ascorbic acid provides incomplete protection, highlighting the need for more effective therapeutic strategies to mitigate alcohol-induced central nervous system damage.