title: [Temporal profile of the superoxide dismutase and the ascorbic acid in focal cerebral ischemia].
abstract: It has been proposed that free radical reactions are involved in ischemic brain damage. Since irreversible pathological changes occurs very early phase of the focal ischemia and the ischemic brain edema reaches its peak at about 2 days of ischemia, the free radical reactions must take place before these changes. Superoxide dismutase is a famous enzyme that dismutase superoxide anion, which is believed to be one of the initiator of the free radical reactions. If superoxide anion plays a pivotal role in the genesis of pathological ischemic brain damage and edema, the activity of the enzyme may decrease in the early phase of ischemia. Ascorbic acid is also known to be a scavenger of superoxide anion, and brain tissue contains it in a high concentration. We investigated the changes in superoxide dismutase activity and concentration of reduced ascorbate in focal ischemia. Focal ischemia was produced in rats by permanent occlusion of the left middle cerebral artery. The animals were decapitated 30 minutes, 4, 24, and 48 hours after the operation. Middle cerebral artery territory of each cerebral hemisphere was homogenized and centrifuged with phosphate buffer. The supernatant was divided into two aliquots; one was dialyzed to remove ascorbate and the other was not. The SOD activity was measured by electron-spin-resonance (ESR) spin trapping method, and the ascorbic acid concentration was measured by high performance liquid chromatography with electrochemical detection (HPLC-ECD). Protein concentration was measured by Lowry's method. The enzyme activity was expressed as unit/mg protein, and the ascorbic acid concentration was expressed as microgram/g tissue. The SOD activity decreased markedly by dialysis.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Neurosurgery, Teikyo University Mizonokuchi Hospital, Kawasaki, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Takagi
authors.forename: H
authors.initials: H
authors.lastname: Kanemitsu
authors.forename: M
authors.initials: M
authors.lastname: Kohno
authors.forename: K
authors.initials: K
authors.lastname: Mitsuda
authors.forename: N
authors.initials: N
authors.lastname: Tomukai
authors.forename: H
authors.initials: H
authors.lastname: Oka
authors.forename: A
authors.initials: A
authors.lastname: Tamura
authors.forename: K
authors.initials: K
authors.lastname: Sano
mesh_terms: D000818:Animals; D001205:Ascorbic Acid / Q000378:metabolism*; D003956:Dialysis; D004195:Disease Models, Animal; D005609:Free Radicals; D002546:Ischemic Attack, Transient / Q000201:enzymology / Q000378:metabolism*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D013482:Superoxide Dismutase / Q000378:metabolism*; D013997:Time Factors
chemical_list: D005609:Free Radicals; D013482:Superoxide Dismutase; D001205:Ascorbic Acid