Document Type : Original Article
1 Department of Anatomy, College of Medicine and Health Sciences, Afe Babalola University, Ado Ekiti, Nigeria
2 Department of Physiology, College of Medicine and Health Sciences, Afe Babalola University, Ado Ekiti, Nigeria
3 Department of Physiology, College of Medicine and Health Sciences, Ahmadu Bello University, Zaria, Nigeria
Objective: This study was to evaluate the effect of Vitamin C on the histology and histochemistry of the prefrontal cortex of ethanol-induced rats. Methods: Male Sprague-Dawley rats were used for the study. Ethical approval was obtained from the University’s ethical committee. The rats were randomly divided into 6 groups of 10 rats each. Rats in group A= free access to normal saline. Rats in group B= treated with 4.25 ml ethanol. Rats in group C= treated with 100 mg/kg Vit. C. Rats in group D= pre-treated with 100 mg/kg Vit. C followed by 4.25 ml ethanol. Rats in group E=co-treated with 100 mg/kg of Vit. C and 4.25ml ethanol. Rats in group F=post-treated with 4.25ml ethanol followed by 100 mg/kg Vit.C. 24hrs after the last administration, the rats were sacrificed by cervical dislocation: the fraction of the brain for tissue histochemistry was fixed in formol calcium and later processed for Heamotoxylin and Eosin with Cresyl fast violent staining techniques and the other fraction meant for enzyme and/or marker histochemistry was processed accordingly for some neurochemical indices for oxidative stress. Results: The markers of oxidative stress were statistically increased in the rats in group D, E and F compared with the rats in group B. There is a significant reduction of TBARS when compared with ethanol induced group (group B). The histological profile of the prefrontal cortex of rats in group A and C were preserved while that of the rats in group B displayed distorted cytoarchitecture profile with a marked increase in apoptotic bodies, lateral deviation of neurons and a marked increase in the activities of oxidative markers.
Gruchow HW, Soboclaski KA, Barboriak JJ (1985). Alcohol consumption, nutrients intake and relative body weight among US adults. Am. J. Clin. Nutr. 42(2):289-295.
Ighodaro OM, Omole JO (2012) Ethanol-induced hepatotoxicity in male wistar rats: effect of aqueous leaf extract of Ocimum gratissimum. Journal of Medicine and Medicinal science Vol 3(8): 499-505
Kubota M, Nakazaki S, Hirai S (2001).Alcohol consumption and frontal lobe shrinkage: Study of 1432 non-alcoholic subjects. J Neurosurg Psychiatry 71:104-6
Lieber CS (2003). Relationships between Nutrition, Alcohol Use and liver disease. Alcohol Health & Research World; 27(3):220-231
Mandi J, Szarka A. and Banhegyi G (2009). Vitamin C: Update on physiology and pharmacology. British Journal of Pharmacology 157:1097-1110
Mcdonough KH (2003). Antioxidant nutrients and alcohol. Toxicology, 189:89-97
Parsons OA (1987) Intellectual impairment in alcoholics: Persistent issues. Acta Med Scand 717 (suppl)33-46
Rukkumani R, Aruna K, Suresh VP, Menon VP (2004). Influence of folic acid on circulatory peroxidantantioxidant status during Alcohol and PUFA-induced
toxicity. J. physiol. Pharmacol. 55(3):551-561
Soujanya S, Lakshman MA, Gopala R (2012) Histopathological and ultrastructural changes induced by imidacloprid in brain and protective role of Vitamin C in rats. Journal.Chemical and Pharmaceutical Research.
Subir KD, Hiran KR, Sukles M and Vasudevan DM (2007). Oxidative stress is the primary event: Effects of ethanol consumption in brain. Ind. J. Clin. Biochem. 22(1)99-104
Sullivian EA, Pfefferbaum A (2005) Neurocircuitry in alcoholism: a substrate of disruption and repair. J.Psychopharmacology 180:583-594
Tsukamoto H, Lu CS (2001). Current concepts in the pathogenesis of alcoholic liver injury. The FASEB J. 15:1335-1349.
Tuma DJ, Casey CA (2003). Dangerous byproducts of alcohol breakdown-focus on adduct Alcohol Health & Research World. 27(4):285-290.
Wu D, Cederbaum AL (2003). Alcohol oxidative stress and Free Radical Damage. Alcohol Res. Health. 27(4):277-284.