Biological Trace Element Research

, Volume 101, Issue 1, pp 73–86

Selenium protects cerebral ischemia in rat brain mitochondria

Authors

  • Mubeen Ahmad Ansari
    • Neurotoxicology Laboratory, Department of Medical Elementology and ToxicologyJamia Hamdard (Hamdard University)
  • Abdullah Shafique Ahmad
    • Neurotoxicology Laboratory, Department of Medical Elementology and ToxicologyJamia Hamdard (Hamdard University)
  • Muzamil Ahmad
    • Neurotoxicology Laboratory, Department of Medical Elementology and ToxicologyJamia Hamdard (Hamdard University)
  • Sofiyan Salim
    • Neurotoxicology Laboratory, Department of Medical Elementology and ToxicologyJamia Hamdard (Hamdard University)
  • Seema Yousuf
    • Neurotoxicology Laboratory, Department of Medical Elementology and ToxicologyJamia Hamdard (Hamdard University)
  • Tauheed Ishrat
    • Neurotoxicology Laboratory, Department of Medical Elementology and ToxicologyJamia Hamdard (Hamdard University)
  • Fakhrul Islam
    • Neurotoxicology Laboratory, Department of Medical Elementology and ToxicologyJamia Hamdard (Hamdard University)
Original Articles

DOI: 10.1385/BTER:101:1:73

Cite this article as:
Ansari, M.A., Ahmad, A.S., Ahmad, M. et al. Biol Trace Elem Res (2004) 101: 73. doi:10.1385/BTER:101:1:73

Abstract

Normal cellular metabolism produces oxidants that are neutralized by the cells' antioxidant enzymes and antioxidants taken from outside. An imbalance between oxidant and antioxidant has been postulated to lead to the neurodegeneration in the ischemic condition. In this study, we have demonstrated the prevention or slowdown of neuronal injury in middle cerebral artery occlusion (MCAO) by sodium selenite. Rats were pretreated with 0.05, 0.1, and 0.2 mg/kg body wt of sodium selenite for 7 d. The rats of group I (sham) and group II (ischemia) were pretreated with physiological saline for 7 d. On d 8, MCAO was induced for 2 h in, the right side of brain of group II, III, IV, and V rats. Brains were dissect out after 22 h of reperfusion and washed with chilled physiological saline. The right cerebral hemisphere was used for the preparation of mitochondria. The activity of superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase, and monoamine oxidase (MAO-A and MAO-B) was depleted significantly; conversely, the activity of poly(ADP-ribosyl) polymerase was elevated significantly as compared to the sham, and the pretreatment of the animals with different doses of sodium selenite has protected the activity of these enzymes significantly. The content of glutathione was decreased significantly, whereas the level of lipid peroxidation was increased significantly in the mitochondria of MCAO as compared to the sham group, and pretreatment with different doses of sodium selenite has protected their levels significantly as compared to the MCAO group. It is concluded that selenium, which is an essential part of our diet, might be helpful in protection against neurodegeneration in cerebral ischemia.

Index Entries

Sodium selenitecerebral ischemiabrain mitochondriaoxidative stressantioxidant enzymeslipid peroxidationmonoamine oxidasepoly(ADP-ribosyl) polymerase
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Copyright information

© Humana Press Inc 2004