allopurinol has been researched along with Parkinson-Disease--Secondary* in 2 studies
2 other study(ies) available for allopurinol and Parkinson-Disease--Secondary
| Article | Year |
|---|---|
Activation of adenosine triphosphate-sensitive potassium channels confers protection against rotenone-induced cell death: therapeutic implications for Parkinson's disease.
It is anticipated that further understanding of the protective mechanism induced by ischemic preconditioning will improve prognosis for patients of ischemic injury. It is not known whether preconditioning exerts beneficial actions in neurodegenerative diseases, in which ischemic injury plays a causative role. Here we show that transient activation of ATP-sensitive potassium channels, a trigger in ischemic preconditioning signaling, confers protection in PC12 cells and SH-SY5Y cells against neurotoxic effect of rotenone and MPTP, mitochondrial complex I inhibitors that have been implicated in the pathogenesis of Parkinson's disease. The degree of protection is in proportion to the bouts of exposure to an ATP-sensitive potassium channel opener, a feature reminiscent of ischemic tolerance in vivo. Protection is sensitive to a protein synthesis inhibitor, indicating the involvement of de novo protein synthesis in the protective processes. Pretreatment of PC12 cells with preconditioning stimuli FeSO(4) or xanthine/xanthine oxidase also confers protection against rotenone-induced cell death. Our results demonstrate for the first time the protective role of ATP-sensitive potassium channels in a dopaminergic neuronal cell line against rotenone-induced neurotoxicity and conceptually support the view that ischemic preconditioning-derived therapeutic strategies may have potential and feasibility in therapy for Parkinson's disease. Topics: Adenosine Triphosphate; Animals; Cell Death; Dose-Response Relationship, Drug; Electron Transport Complex I; Ferrous Compounds; Glyburide; Ischemic Preconditioning; Mitochondria; NADH, NADPH Oxidoreductases; Neurons; Parkinson Disease; Parkinson Disease, Secondary; PC12 Cells; Pinacidil; Potassium Channel Blockers; Potassium Channels; Protein Synthesis Inhibitors; Rats; Rotenone; Uncoupling Agents; Vasodilator Agents; Xanthine; Xanthine Oxidase | 2002 |
Allopurinol suppresses para-nonylphenol and 1-methyl-4-phenylpyridinium ion (MPP(+))-induced hydroxyl radical generation in rat striatum.
We recently demonstrated that para-nonylphenol, an environmental estrogen-like chemical, enhances hydroxyl radical (*OH) generation in the rat striatum. In the present study we have examined whether para-nonylphenol enhanced 1-methyl-4-phenylpyridinium ion (MPP(+))-induced *OH generation in the rat striatum using a microdialysis technique. Para-nonylphenol significantly enhanced MPP(+)-induced *OH generation. Further, we studied the effect of allopurinol, a xanthine oxidase inhibitor, on para-nonylphenol and MPP(+)-induced *OH generation. Allopurinol significantly suppressed para-nonylphenol and MPP(+)-induced *OH generation. The results indicate that para-nonylphenol enhanced *OH generation based on superoxide anion production, and allopurinol may have preventive effect on para-nonylphenol and MPP(+)-induced *OH generation. Topics: 1-Methyl-4-phenylpyridinium; Allopurinol; Animals; Dose-Response Relationship, Drug; Drug Interactions; Free Radical Scavengers; Hazardous Substances; Hydroxyl Radical; Male; Microdialysis; Neostriatum; Nerve Degeneration; Parkinson Disease; Parkinson Disease, Secondary; Phenols; Rats; Rats, Wistar | 2001 |