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Mohsenikia M et al. g/dL) was significantly lower than those of the group A (7.114 ± 154) and the group C (5.930 ± 201, P < 0.05). Also there was a significant difference between the group B and the group C (P < 0.05). Albumin level in the group B (3.012 ± 0.181 g/dL) was significantly lower than those of the group A (4.264 ± 0.251) and the group C (3.546 ± 234, P < 0.05). Moreover, there was a significant difference between the group B and the group C (P < 0.05). Triglyceride level in the group B (119.900 ± 6.279 mg/dL) was significantly higher than those of the group A (71.314 ± 4.516) and the group C (91.266 ± 5.046, P < 0.05). Also, there was a significant difference between the group B and the group C (P < 0.05). 5. Discussion The process of CsA-induced hepatotoxicity begins with degradation of arachidonic acid, synthesis of eicosanoids and release of free radicals (as hydroxyl radical) that initiate lipid peroxidation and the secondary activation of physiologic antioxidant defenses. In prior studies, changes in the activities of antioxidant enzymes (lowered SOD, and increased CAT activities) and observed increase in peroxidation products in the liver tissues from cyclosporine-treated rabbits have been established (11). Our study shows that there were significant increases in ALT, AST, bilirubin, LDM, ALP and triglyceride levels in plasma, and significant decrease in total protein and albumin level of the plasma in the group B and the group C but the amount of increase between group B and C was also significant. Vitamin C treatment significantly decreased liver toxicity against CsA-induced plasma biochemical changes. The results in this experiment recommend that vitamin C be effective in decreasing the CsA-induced hepatotoxicity; however, level of ALT, AST, bilirubin, LDM, ALP and triglyceride in the group C was higher than that of the group A and the level of total protein and Albumin was lower than that of the group A significantly. Our results approve the results of Benito B (12) report in which studied effect of vitamin C in liver protein pattern of CsA-treated rats. Although this study shows the beneficial effect of vitamin C in decreasing CsA-induced liver toxicity it has been suggested that antioxidant supplementation is beneficial only when elevated oxidative stress is present (13) because some studies show that the co-administration of antioxidants like vitamin C may decrease CsA dose in the body and interfere with the aim of using CsA regimen in patients (14). In conclusion, we have shown that vitamin C administration provides pro- Prophylactic Effect of Vitamin C tection against CsA-induced injury in rat liver function and it may have hepatoprotective role in patients experiencing CSA treatment. Acknowledgments None declared. Financial Disclosure None declared. Funding/Support None declared. References 1. Kahan BD. Immunosuppressive therapy. Curr Opin Immunol. 1992;4(5):553-60. 2. Rezzani R. Cyclosporine A and adverse effects on organs: histochemical studies. Prog Histochem Cytochem. 2004;39(2):85-128. 3. Wolf A, Trendelenburg CF, Diez-Fernandez C, Prieto P, Houy S, Trommer WE, et al. Cyclosporine A-induced oxidative stress in rat hepatocytes. J Pharmacol Exp Ther. 1997;280(3):1328-34. 4. Moran D, De Buitrago JM, Fernandez E, Galan AI, Munoz ME, Jimenez R. Inhibition of biliary glutathione secretion by cyclosporine A in the rat: possible mechanisms and role in the cholestasis induced by the drug. J Hepatol. 1998;29(1):68-77. 5. Galan AI, Munoz ME, Jimenez R. S-Adenosylmethionine protects against cyclosporin A-induced alterations in rat liver plasma membrane fluidity and functions. J Pharmacol Exp Ther. 1999;290(2):774-81. 6. Durak I, Ozbek H, Elgun S. Cyclosporine reduces hepatic antioxidant capacity: protective roles of antioxidants. Int Immunopharmacol. 2004;4(3):469-73. 7. Greene EL, Paller MS. Oxygen free radicals in acute renal failure. Miner Electrolyte Metab. 1991;17(2):124-32. 8. Valko M, Rhodes CJ, Moncol J, Izakovic M, Mazur M. Free radicals, metals and antioxidants in oxidative stress-induced cancer. Chem Biol Interact. 2006;160(1):1-40. 9. Suh J, Zhu BZ, Frei B. Ascorbate does not act as a pro-oxidant towards lipids and proteins in human plasma exposed to redoxactive transition metal ions and hydrogen peroxide. Free Radic Biol Med. 2003;34(10):1306-14. 10. Podmore ID, Griffiths HR, Herbert KE, Mistry N, Mistry P, Lunec J. Vitamin C exhibits pro-oxidant properties. Nature. 1998;392(6676):559. 11. Durak I, Kacmaz M, Cimen MY, Buyukkocak S, Elgun S, Ozturk HS. The effects of cyclosporine on antioxidant enzyme activities and malondialdehyde levels in rabbit hepatic tissues. Transpl Immunol. 2002;10(4):255-8. 12. Benito B, Wahl D, Steudel N, Cordier A, Steiner S. Effects of cyclosporine A on the rat liver and kidney protein pattern, and the influence of vitamin E and C coadministration. Electrophoresis. 1995;16(7):1273-83. 13. Jialal I, Devaraj S. Antioxidants and atherosclerosis: don’t throw out the baby with the bath water. Circulation. 2003;107(7):926-8. 14. Blackhall ML, Fassett RG, Sharman JE, Geraghty DP, Coombes JS. Effects of antioxidant supplementation on blood cyclosporin A and glomerular filtration rate in renal transplant recipients. Nephrol Dial Transplant. 2005;20(9):1970-5. 26 Thrita Stud J Med Sci. 2012;1(1):24-26
KOWSAR Thrita Stud J Med Sci.2012;1(1):27-29. DOI: 105812/Thrita.4265 Student Journal of Medical Sciences Thritajournal.com Antiepileptic Effect of Vitamin E on Kainic Acid-induced Temporal Lobe Epilepsy in Rats Zahra Kiasalari 1* , Mehrdad Roghani 1 , Mohsen Khalili 1 , Samaneh Shafii 1 1 Department of physiology, School of Medicine and Neurophysiology Research Center, Shahed University, Tehran, IR Iran ARTICLE INFO ABSTRACT Article type: Original Article Article history: Received: 17 Aug 2011 Revised: 11 Sep 2011 Accepted: 5 Nov 2011 Keywords: Vitamin E Valproic acid Epilepsy, temporal lobe Convulsion Anticonvulsants Background: Epilepsy is a chronic neurological disease with the prevalence of around one percent. Despite the introductions of several anti-epileptic drugs, around 1/3 of epileptic patients are resistant to the anti-epileptic medications. Considering the evidence regarding the anti-oxidant action of Vitamin E and its beneficiary effect in the treatment of epilepsy, we investigated the anti-convulsive effect of Vitamin E in a rat model of kainic acid-induced epilepsy. Materials and Methods: Forty male rats were divided to five groups (sham, Vit E, epileptic, epileptic treated with Vit E and epileptic treated with valproic acid). Epilepsy was induced by intra hippocampal injection of 4 microgram of kainic acid. Rats receiving daily intraperitoneal injections of Vit E (100 mg/kg) or valproic acid (200 mg/kg) in the week preceding the surgery. Intensity of epileptic convulsions was graded using Racine’s criteria. Results: No convulsions were observed in the sham-Vit E groups. Widespread convulsions were observed in the kainic acid-treated group. Intensity of convulsions were significantly reduced in the epileptic rats receiving either Vit E or valproic acid (P < 0.05 and P < 0.01, respectively). Conclusions: Pre-treatment with Vit E decreases the convulsion intensity in kainic acidinduced epilepsy in rats. Copyright c 2012 Kowsar M. P. Co. All rights reserved. Implication for health policy/practice/research/medical education: Reading of time article is recommended for neurologists, basic scientists and those who are involved in the treatment of epilepic patients. Please cite this paper as: Kiasalari Z, Roghani M, Khalili M, Shafii S. Anti–epileptic Effect of Vit E on rat Kainic Acid-induced Temporal Lobe Epilepsy. Thrita Stud J Med Sci. 2012;1(1):27-9. DOI: 105812/Thrita.4265 1. Background Epilepsy is the most common neurological disorder after stroke and Alzheimer disease; approximately one percent of world population is suffering from one type of epilepsy disorder (1). Epileptic seizures are generally divided into two categories: focal and generalized. Temporal lobe epilepsy is the most common focal seizure * Corresponding author: Zahra Kiasalari, Department of Physiology, School of Medicine, Shahed University, Dehkadeh Street, Keshavarz Blvd., P.O. Box 14155-7435, Tehran, IR Iran. Tel: +98-2188964792, Fax: +98-2188966310. E-mail: kiasalari@yahoo.com DOI: 105812/Thrita. 4265 Copyright c 2012 Kowsar M.P.Co. All rights reserved. subtype in adults which results from repeated-release foci in medial temporal structures such as hippocampus and amygdale and is associated with hippocampal degeneration and related functional changes (2). Epilepsy is associated with a specific structural lesion in the hippocampus, which may be surgically resected in medically intractable cases. Investigation of temporal lobe epilepsy is stimulated, in part, by the involvement of the hippocampus which has a simple organization compared with other parts of the cerebral cortex and plays a role in learning and memory (2). Insights gained from studying temporal lobe epilepsy may be applied to other types of epilepsy and help reveal mechanisms of tempo-
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