title: L-deprenyl reduces brain damage in rats exposed to transient hypoxia-ischemia.
abstract: OBJECTIVE
  L-Deprenyl (Selegiline) protects animal brains against toxic substances such as 1-methyl-1,2,3,6-tetrahydropyridine and 6-hydroxydopamine. Experiments were conducted to test whether L-deprenyl prevents or reduces cerebral damage in a transient hypoxia/ischemia rat model.
  
  
  METHODS
  Rats were treated for 14 days with 2 mg/kg and 10 mg/kg L-deprenyl or saline. After surgery a 20-minute hypoxia/ischemia period was induced by simultaneous occlusion of the left common carotid artery and reduction of the percentage of oxygen in the gas mixture to 10%. Rats were killed 24 hours later. Silver staining was used to reveal damage in several brain regions.
  
  
  RESULTS
  In the brain, both L-deprenyl dosages reduced damage up to 78% compared with the controls. Total brain damage was decreased from 23%-31% to 5%-9% with the L-deprenyl treatment (2 mg/kg: F1.13 = 6.956, P < .05; 10 mg/kg: F1.13 = 5.731, P < .05). In the striatum, significant treatment effects were found between both the L-deprenyl groups (2 mg/kg and 10 mg/kg, respectively) and the saline group (F1.13 = 14.870, P < .005; and F1.13 = 8.937, P = .01; respectively). In the thalamus, significant treatment effects were seen in the 2-mg/kg L-deprenyl group (F1.13 = 11.638, P < .005) and the 10-mg/kg group (F1.13 = 8.347, P < .05) compared with the control group. No significant damage decrease was seen in the hippocampus and the cortex.
  
  
  CONCLUSIONS
  The results show that L-deprenyl is effective as a prophylactic treatment for brain tissue when it is administered before hypoxia/ischemia. Mechanisms responsible for the observed protection remain unclear. The regional differences in damage, however, are in accordance with the reported regional increase in superoxide dismutase and catalase activities after L-deprenyl treatment, suggesting the involvement of free radicals and scavenger enzymes.
authors.affiliation: University of Groningen, Department of Biological Psychiatry, The Netherlands.
authors.forename: S
authors.initials: S
authors.lastname: Knollema
authors.forename: W
authors.initials: W
authors.lastname: Aukema
authors.forename: H
authors.initials: H
authors.lastname: Hom
authors.forename: J
authors.initials: J
authors.lastname: Korf
authors.forename: G J
authors.initials: GJ
authors.lastname: ter Horst
mesh_terms: D000818:Animals; D001921:Brain / Q000187:drug effects / Q000473:pathology; D002374:Catalase / Q000378:metabolism; D002540:Cerebral Cortex / Q000187:drug effects / Q000473:pathology; D003342:Corpus Striatum / Q000187:drug effects / Q000473:pathology; D006624:Hippocampus / Q000187:drug effects / Q000473:pathology; D002534:Hypoxia, Brain / Q000473:pathology / Q000517:prevention & control*; D002546:Ischemic Attack, Transient / Q000473:pathology / Q000517:prevention & control*; D008297:Male; D008996:Monoamine Oxidase Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use*; D018696:Neuroprotective Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D016548:Prosencephalon / Q000187:drug effects / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D012642:Selegiline / Q000008:administration & dosage / Q000627:therapeutic use*; D013482:Superoxide Dismutase / Q000378:metabolism; D013788:Thalamus / Q000187:drug effects / Q000473:pathology
chemical_list: D008996:Monoamine Oxidase Inhibitors; D018696:Neuroprotective Agents; D012642:Selegiline; D002374:Catalase; D013482:Superoxide Dismutase