A synthetic human proline-rich-polypeptide enhances hydroxyl radical generation and fails to protect dopaminergic neurons against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced toxicity in mice.
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| 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 microg/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.
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| Authors | Varduhi H Knaryan, Supriti Samantaray, Armen A Galoyan, Kochupurackal P Mohanakumar |
| Journal | Neuroscience letters (Neurosci Lett) Vol. 375 Issue 3 Pg. 187-91 (Mar 03 2005) ISSN: 0304-3940 [Print] Ireland |
| PMID | 15694258 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't) |
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