title: Selenium protects cerebral ischemia in rat brain mitochondria.
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.
authors.affiliation: Neurotoxicology Laboratory, Department of Medical Elementology and Toxicology, Jamia Hamdard, Hamdard University, Hamdard Nagar, New Delhi-110062, India.
authors.forename: Mubeen Ahmad
authors.initials: MA
authors.lastname: Ansari
authors.forename: Abdullah Shafique
authors.initials: AS
authors.lastname: Ahmad
authors.forename: Muzamil
authors.initials: M
authors.lastname: Ahmad
authors.forename: Sofiyan
authors.initials: S
authors.lastname: Salim
authors.forename: Seema
authors.initials: S
authors.lastname: Yousuf
authors.forename: Tauheed
authors.initials: T
authors.lastname: Ishrat
authors.forename: Fakhrul
authors.initials: F
authors.lastname: Islam
mesh_terms: D000818:Animals; D001921:Brain / Q000166:cytology / Q000187:drug effects* / Q000201:enzymology; D002545:Brain Ischemia / Q000188:drug therapy*; D004305:Dose-Response Relationship, Drug; D005978:Glutathione / Q000032:analysis; D020244:Infarction, Middle Cerebral Artery / Q000517:prevention & control*; D008297:Male; D008928:Mitochondria / Q000201:enzymology / Q000378:metabolism*; D008996:Monoamine Oxidase Inhibitors / Q000378:metabolism; D011065:Poly(ADP-ribose) Polymerases / Q000378:metabolism; D051381:Rats; D018038:Sodium Selenite / Q000627:therapeutic use*; D013858:Thiobarbiturates / Q000032:analysis
chemical_list: D008996:Monoamine Oxidase Inhibitors; D013858:Thiobarbiturates; D011065:Poly(ADP-ribose) Polymerases; D005978:Glutathione; D018038:Sodium Selenite