Re: Performance enhancement with selegiline

From: gts (gts_2000@yahoo.com)
Date: Sat Feb 08 2003 - 04:47:47 MST

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    Here is more evidence of neuroprotection by selegiline/deprenyl:

    This is evidence that selegiline protects neurons from death due to from
    temporary lack of oxygen (hypoxia) as in stroke (ischemia).

    ABSTRACT
    L-deprenyl reduces brain damage in rats exposed to transient
    hypoxia-ischemia.

    Stroke 1995 Oct;26(10):1883-7 (ISSN: 0039-2499)
    Knollema S; Aukema W; Hom H; Korf J; ter Horst GJ
    University of Groningen, Department of Biological Psychiatry, The
    Netherlands.
    BACKGROUND AND PURPOSE: 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.



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