Article ID Journal Published Year Pages File Type
9429591 Neuroscience Letters 2005 5 Pages PDF
Abstract
Some of the proline-rich-polypeptides (PRPs) are shown to afford protection against spinal cord transection or crush syndrome-induced neurodegeneration in the brain. In the present study a synthetic proline-rich-polypeptide of human hypothalamus origin (h-PRP) has been examined for its potency to protect against dopaminergic neuronal damage caused by the parkinsonian neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Effect of h-PRP on hydroxyl radical (OH) generation in a Fenton-like reaction was monitored, employing a sensitive salicylate hydroxylation procedure. Balb/c mice treated twice with MPTP (30 mg/kg. i.p., twice, 16 h apart) or h-PRP (20 μg/animal, twice, 16 h apart) showed significant loss of striatal dopamine as assayed by HPLC with electrochemical detection. h-PRP pretreatment failed to attenuate MPTP-induced striatal dopamine depletion. A dose-dependent increase in the generation of OH by h-PRP suggests its pro-oxidant action, and explains its failure to protect against MPTP-induced parkinsonism in mice.
Related Topics
Life Sciences Neuroscience Neuroscience (General)
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