Abstract
In our experimental hypoxia/ischemia (Levine) model several potential protective pretreatments (1—3) were tested on their ability to reduce damage and L-deprenyl (selegiline) proved to be a very effective neuroprotective agent as it is in reducing brain damage when it is applied for 14 days prior to hypoxia/ischemia (4,5). The mechanism through which L-deprenyl diminishes damage is unclear. However, a few obvious possibilities for the protective effects of L-deprenyl should be taken into consideration. First of all the regional differences in damage protection by L-deprenyl (4) is in agreement with MAO-B independent effects of L-deprenyl on free radical scavenger enzymes i.e. catalase and SOD (6,7). The ability of these scavenger enzymes to protect against ischemia induced damage has been described by numerous studies. Especially intrinsically increased expression of the scavenger enzymes had beneficial effects on damage outcome. For instance an increased SOD-expression in transgenic mice offered protection against radicals generated through ischemia (8,9) and/or MPTP (10).
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Knollema, S., Wiersma, A., Ter Horst, G.J. (1997). L-Deprenyl Reduces Brain Damage in the Caudate Putamen by a Mao-Dependent Effect. In: Teelken, A., Korf, J. (eds) Neurochemistry. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5405-9_14
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