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Volume 13
Issue 4
Online publication date 2012-12-15
Title Preventive activity of ascorbic acid on lead acetate induced cerebellar damaged in adult Wistar rats
Author Sunday Abraham Musa, Iliyasu, Musa Omoniye, Wilson Oliver Hamman, Augustine Oseloka Ibegbu, Uduak Emmanuel Umana
Among the environmental contaminants, lead is one of the most hazardous to living matter. In mammals, the main target is the central nervous system, particularly in the young. Ascorbic acid is an antioxidant which is a substance that may protect your cells against the effects of free radicals. 
This study investigated Experiment the protective effect of ascorbic acid on the cerebellum of adult Wistar rats following oral administration of different doses of Lead acetate. Thirty adult Wistar rats of average weight of 215g were used in this study. The animals were divided into five (5) groups of six animals per group and were administered different doses of lead acetate (60mg/kg bwt of 1/10th LD50 and 30mg/kg bwt of 1/20th of LD50) and ascorbic acid (4.3mg/kg bwt) orally over a period of three (3) weeks.
Group 1 (control) was administered distilled water and Group 2 and 3 were administered 30mg/kg and 60mg/kg of Lead acetate respectively while Group 4 and 5 were given co-administration of 30mg/kg of Lead acetate 4.3mg/kg of ascorbic acid and 60gm/kg of Lead acetate 4.3mg/kg of ascorbic acid respectively. Histopathologically, Lead acetate induced cellular damage in the cerebellum of adult Wistar rats and it was also observed that ascorbic acid prevents or minimize lead-induced  cellular damage in the cerebellum of adult Wistar rats.

Bielski, B., 1982. “Chemistry of ascorbic acid radicals,” in: Seiob, P. and Tolbert, B. (eds.), Ascorbic acid: Chemistry, metabolism and uses, Washington DC: American Chem. Soc., pp.81-100

Bodannes, R., Chann, P., 1979. “Ascorbic acid as a scavenger of singlet oxygen,” FFBS Letter, Vol.105, pp.195-96

Bolognesi, C., Morasso, G., 2000. “Genotoxicity of pesticides: Potential risk for consumers,” Trends in Food Science and Technology, Vol.11(4-5), pp.182-87

Canfield, R., Henderson, C., Slechta, D., Cox, C., Jusko, T. and Lanphear, B., 2003. “Intellectual impairment in children with blood lead concentrations below 10µg per decilitre,” The New England Journal of Medicine, Vol.348(16), pp.1517-526

Carr, A., Zhu, B., Frei, B., 2000. “Potential antiatherogenic mechanisms of ascorbate and alpha-tocopherol,” Circulation Research, Vol.87, pp.349-54

Chihuailaf, R., Contreras, P., Wittwer, F., 2002. “Pathogenesis of oxidative stress: Consequences and evaluation in animal health,” Vet Mex., Vol.33(3), pp.265-83

Elombah. com and HRW. (2012). Nigeria’s Child Lead Poisoning Crisis is ‘worst in modern history’ HRW.

Fredericks, CM.,  2011. “Disorders of the cerebellum and its connections,” in: Saladin LK, Fredericks CM, Pathophysiology of the motor systems: principles and clinical presentations, Philadelphia: F.A. Davis, pp.445-66

Halliwell, B., 2001. “Role of free radicals in the neurodegenerative diseases: Therapeutic implications for antioxidant treatment,” Drugs Ageing, Vol.18(9), pp.685-716

Hemila, H., Roberts, P., Wikstrom, M., 1985. “Activated polymorphonuclear leucocytes consume vitamin C,” FEBS Letter, Vol.178, pp.25-30

John, H., Cheryl, H., Richard, S., Christine, S., 1991. Toxics: A to Z - A guide to everyday pollution hazards, Berkeley: University of California Press

Martin, R., Paul, M., Thomas, W., 1970. An Appraisal of Rodent models of lead encephalopathy. In neurotoxicology, Vol.1 edited by Leon, R. and Hirotsugu, S., New York: Raven press

Maurice, V. and James, A., 1972. The nutritional and metabolic diseases of the cerebellum. Clinical and pathological aspects. In the cerebellum in health and diseases, edited by: William, S. and William, D., London: Adam Hilger, pp.412-49

Needleman, H., Schell, A., Bellinger, D., Leviton, A., Allred, E., 1990. “The long-term effects of exposure to low doses of lead in childhood: An 11-year follow-up report,” The New England Journal of Medicine, Vol.322(2), pp.83-88

Nishikimi, M., 1975. “Oxidation of ascorbic acid with superoxide anion generated by thexanthine-xanthine oxidase system,” Biochemistry and Biophysics Research Communication, Vol.63, pp.463-68

Ruff, H., Markowitz, M., Bifur, P., 1996. “Relationships among blood lead levels, iron deficiency, and cognitive development in two-year-old children,” Envoron. Health Perspect., Vol.104(2), pp.180-85 

Satija, N., Vij, A., 1995. “Preventive action of zinc against lead toxicity,” India Journal of Physiol Pharmacol, Vol.39, pp.377-82

Sies, H., Stahi, K., Sundqwist, A., 1992. “Antioxidant functions of vitamins vitamin E and C, betacarotene, and other carotenoids,” Annals of New York Academy of Science, Vol.669, pp.7-20

Srianujata, S., 1997. “Lead, the toxic mental to stay with human,” Journal of Toxicological Sciences, Vol.23, pp.237-40

Sujatha, K., Srilatha, C., Anjaneyulu, Y., Amaravathi, P., 2011. “Lead acetate induced neurotoxicity in wistar albino rats: A pathological, immunological, and ultrastructural studies,” Journal of pharma and bio science Vol.2, pp.459-62

Tong, S., Von Schirnding, Y., Prapamontol, T., 2000. “Environmental lead exposure: A public health problem of global dimensions,” Bulletin WHO, Vol.78(9), pp.1068-1077 

Wright, N., Thacher, T., Pfitzner, M., Fischer, P., Pettifor, J., 2005. “Causes of lead toxicity in a Nigerian city,” Archives of Disease in Childhood, Vol.90(3), pp.262-66

Keywords Lead acetate, ascorbic acid, cellular, cerebellar damage
Pages 99-104
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