EFFECT OF SOME LOW MOL TRAUM *1 Suleiman, N., 2 Bilbis, L. S., 2 Sai 6 Garb 1 Departme 3 Depart 4 Department of Che 5 Departme 6 Department V 7 Department of Veterinary 8 Department of Veterinary Physiolo ARTICLE INFO ABST Excess defens events mass a acceler molecu perform analyz indicat and gl (MDA the hea non-tre groups and m trauma Copyright © 2015 Suleiman et al. This is an open acc distribution, and reproduction in any medium, provided INTRODUCTION Traumatic brain injury (TBI) is a worldwid management can pose enormous challeng delivery as well as significantly stretch resources including manpower and facilitie and Allison, 2010). In Africa, road traffic responsible for the majority of head and sp causing 80% of all injuries in Nigeria alon from RTAs is higher than those of both the other developing countries (Awojebi, 1987) poor road network and recklessness in drivin *Corresponding author: Suleiman, N., Department of Veterinary Physiology and Biochem ISSN: 0975-833X Article History: Received 05 th April, 2015 Received in revised form 11 th May, 2015 Accepted 22 nd June, 2015 Published online 31 st July, 2015 Key words: Oxidativestress, Traumatic brain injury, Antioxidants, Modified Glasgow coma scale. Citation: Suleiman, N., 2 Bilbis, L.S., Saidu, Y., of traumatic Brain injury in albino rats”, Internat RESEARCH ARTICLE LECULAR MASS ANTIOXIDANTS IN THE M MATIC BRAIN INJURY IN ALBINO RATS idu, Y., 3 Nasiru, J. I., 4 Dallatu, M. K., 5 Saha ba, B., 7 Yakubu, A. S. and 8 Bulama, I. ent of Veterinary Physiology and Biochemistry 2 Department of Biochemistry tment of Surgery, College of Health Science emical Pathology, Faculty of Medical Laborator ent of Histopathology, College of Health Science Veterinary Public Health and Preventive Medic y Surgery and Radiology, Usmanu Danfodiyo Un ogy, Pharmacology and Biochemistry, Universi TRACT sive generation of reactive oxygen species (ROS) and imp se mechanism begins immediately after traumatic brain in leading to neuronal dysfunction and death. This study repo antioxidantsin the management of TBI. Winstar rats subjec rated impact device were administered 22.5mg/kg and 45mg ular mass antioxidants (LMMA) for two weeks. Modified med to ascertain the level of consciousness. Blood and zed for oxidative stress biomarkers and histological app ted that TBI caused significant decrease (P<0.05) superoxid lutathione peroxidase (GPx) activities, and significantly i A) concentration. Supplementation with some LMMA howev aling time and mortality. Histology also showed interparan eated rats group, and healing/normal brain sections in t s. Supplementation of antioxidants to TBI induced rats red may be responsible for the observed reduction in morta atised rats. cess article distributed under the Creative Commons Attribution L the original work is properly cited. de problem and its ge to health care hing the hospital es (Eghwrudjakpor accident (RTA) is pinal cord injuries ne. Nigeria’s death e industralised and ), probably due to ng. mistry Two different mechanisms usu TBI. The primary insult occurr followed by the secondary p oxidative stress (Ferguson et a has been implicated as potentia of acute central nervous sy significant role in secondary d mortality following TBI(Coo principally susceptible to OS oxidative metabolic activity, in reactive oxygen metabolites replicating nature of neurons, a ratio (Evans 1993). Antioxid scavengers can, therefore, pro Available online at http://www.journalcra.com International Journal of Current Research Vol. 7, Issue, 07, pp.18492-18499, July, 2015 I Nasiru, J.I et al, 2015. “Effect of some low molecular mas tional Journal of Current Research, 7, (7), 18492-18499. MANAGEMENT OF abi, S. M., 4 Ngaski A. A., y ry Science e cine University Sokoto ity of Maiduguri, Nigeria pairment of endogenous antioxidant njury (TBI), resulting in secondary orts the role of some low molecular cted to closed head injury using an g/kg body weight of some of the low Glasgow coma scale (MGCS) was d brain tissues were collected and pearances respectively. The results de dismutase (SOD), catalase (CAT) increase (P<0.05) malondialdehyde ver reverted the trend and decreased nchymal hemorrhage in traumatized- the TBI antioxidants supplemented duced the impact of oxidative stress ality rate and healing time in the License, which permits unrestricted use, ually determine the damage after ring immediately after the injury, pathological processes such as al., 2010). Oxidative stress (OS) al contributor to the pathogenesis ystem (CNS) injury, it has a damage, and it is responsible for ok et al., 2010). The brain is S because of its high rate of ntense or extreme production of (Ames et al., 1993), non- and high membrane-to-cytoplasm dants known to be free-radical otect against per oxidative tissue INTERNATIONAL JOURNAL OF CURRENT RESEARCH ss antioxidants in the management