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Effects of α-tocopherol and ascorbic acid in the severity and management of traumatic brain injury in albino rats
BACKGROUND: Traumatic brain injury (TBI) is accompanied by substantial accumulation of biomarkers of oxidative stress and depletion of antioxidants reserve which initiate chain reactions that damage brain cells. The present study investigated the role of ascorbic acid and α-tocopherol on the severit...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Medknow Publications & Media Pvt Ltd
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3821415/ https://www.ncbi.nlm.nih.gov/pubmed/24250162 http://dx.doi.org/10.4103/0976-3147.118784 |
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author | Ishaq, Gaafar M. Saidu, Yusuf Bilbis, Lawal S. Muhammad, Suleiman A. Jinjir, Nasir Shehu, Bello B. |
author_facet | Ishaq, Gaafar M. Saidu, Yusuf Bilbis, Lawal S. Muhammad, Suleiman A. Jinjir, Nasir Shehu, Bello B. |
author_sort | Ishaq, Gaafar M. |
collection | PubMed |
description | BACKGROUND: Traumatic brain injury (TBI) is accompanied by substantial accumulation of biomarkers of oxidative stress and depletion of antioxidants reserve which initiate chain reactions that damage brain cells. The present study investigated the role of ascorbic acid and α-tocopherol on the severity and management of TBI in rats. MATERIALS AND METHODS: Wistar rats were subjected to closed head injury using an accelerated impact device. Rats were administered 45 mg/kg and 60 mg/kg body weight of ascorbic acid, α-tocopherol or a combination of the two vitamins for 2 weeks pre- and post injury. Blood and brain tissue homogenates were analyzed for vitamin C, vitamin E, malondialdehyde, superoxide dismutase, and creatine kinase activities. RESULTS: The results indicated that TBI caused significant (P < 0.05) decreased in vitamins C and E levels in the blood and brain tissue of TBI-untreated rats. The activities of superoxide dismutase in TBI rats were markedly reduced when compared with non traumatized control and showed a tendency to increased following supplementation with vitamins C and E. Supplementation of the vitamins significantly (P < 0.05) reduced malondialdehyde in the treatment groups compared with the TBI-untreated group. CONCLUSION: The study indicated that pre and post treatment with ascorbic acid and α-tocopherol reduced oxidative stress induced by brain injury and effectively reduced mortality rate in rats. |
format | Online Article Text |
id | pubmed-3821415 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Medknow Publications & Media Pvt Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-38214152013-11-18 Effects of α-tocopherol and ascorbic acid in the severity and management of traumatic brain injury in albino rats Ishaq, Gaafar M. Saidu, Yusuf Bilbis, Lawal S. Muhammad, Suleiman A. Jinjir, Nasir Shehu, Bello B. J Neurosci Rural Pract Original Article BACKGROUND: Traumatic brain injury (TBI) is accompanied by substantial accumulation of biomarkers of oxidative stress and depletion of antioxidants reserve which initiate chain reactions that damage brain cells. The present study investigated the role of ascorbic acid and α-tocopherol on the severity and management of TBI in rats. MATERIALS AND METHODS: Wistar rats were subjected to closed head injury using an accelerated impact device. Rats were administered 45 mg/kg and 60 mg/kg body weight of ascorbic acid, α-tocopherol or a combination of the two vitamins for 2 weeks pre- and post injury. Blood and brain tissue homogenates were analyzed for vitamin C, vitamin E, malondialdehyde, superoxide dismutase, and creatine kinase activities. RESULTS: The results indicated that TBI caused significant (P < 0.05) decreased in vitamins C and E levels in the blood and brain tissue of TBI-untreated rats. The activities of superoxide dismutase in TBI rats were markedly reduced when compared with non traumatized control and showed a tendency to increased following supplementation with vitamins C and E. Supplementation of the vitamins significantly (P < 0.05) reduced malondialdehyde in the treatment groups compared with the TBI-untreated group. CONCLUSION: The study indicated that pre and post treatment with ascorbic acid and α-tocopherol reduced oxidative stress induced by brain injury and effectively reduced mortality rate in rats. Medknow Publications & Media Pvt Ltd 2013 /pmc/articles/PMC3821415/ /pubmed/24250162 http://dx.doi.org/10.4103/0976-3147.118784 Text en Copyright: © Journal of Neurosciences in Rural Practice http://creativecommons.org/licenses/by-nc-sa/3.0 This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Ishaq, Gaafar M. Saidu, Yusuf Bilbis, Lawal S. Muhammad, Suleiman A. Jinjir, Nasir Shehu, Bello B. Effects of α-tocopherol and ascorbic acid in the severity and management of traumatic brain injury in albino rats |
title | Effects of α-tocopherol and ascorbic acid in the severity and management of traumatic brain injury in albino rats |
title_full | Effects of α-tocopherol and ascorbic acid in the severity and management of traumatic brain injury in albino rats |
title_fullStr | Effects of α-tocopherol and ascorbic acid in the severity and management of traumatic brain injury in albino rats |
title_full_unstemmed | Effects of α-tocopherol and ascorbic acid in the severity and management of traumatic brain injury in albino rats |
title_short | Effects of α-tocopherol and ascorbic acid in the severity and management of traumatic brain injury in albino rats |
title_sort | effects of α-tocopherol and ascorbic acid in the severity and management of traumatic brain injury in albino rats |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3821415/ https://www.ncbi.nlm.nih.gov/pubmed/24250162 http://dx.doi.org/10.4103/0976-3147.118784 |
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