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|Title:||1-Methyl-4-phenyl-pyridinium ion-induced oxidative stress, c-Jun phosphorylation and DNA fragmentation factor-45 cleavage in SK-N-SH cells are averted by selegiline|
The Institute of Science and Technology for Research and Development, Mahidol University
University of North Dakota
|Keywords:||Biochemistry, Genetics and Molecular Biology;Neuroscience|
|Citation:||Neurochemistry International. Vol.53, No.6-8 (2008), 283-288|
|Abstract:||Parkinson's disease is a progressive neurodegenerative disorder, associated with the selective loss of dopaminergic neurons in the substantia nigra pars compacta. Recent studies have shown that c-Jun-N terminal kinase pathways might be involved in the oxidative stress-induced neuronal demise. In addition, there are several studies demonstrating that selegiline protects neural cell degeneration. In view of the above, the toxic effects of MPP+and the protective roles of selegiline were studied in cultures of human neuroblastoma (SK-N-SH) cell lines in the present study. MPP+significantly decreased cell viability but increased reactive oxygen species formation and lipid peroxidation, and the said effects were attenuated by selegiline. MPP+did not change the total levels of c-Jun but enhanced phosphorylation of c-Jun at Ser73 and cleavage of DNA fragmentation factor 45, which were diminished by selegiline. MPP+-treated SK-N-SH cells exhibited an irregularly shaped nuclear chromatin or DNA fragmentation, which was abolished by selegiline. These data suggest that c-Jun-N terminal kinase pathways are involved in oxidative stress-induced dopaminergic neuronal degeneration and pretreatment with selegiline affords neuroprotection by inhibiting these cell death-signaling pathways. © 2008 Elsevier Ltd. All rights reserved.|
|Appears in Collections:||Scopus 2006-2010|
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