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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.
Neurochem Int. 2008 Dec; 53(6-8):283-8.NI

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.

Authors+Show Affiliations

Institute of Science and Technology for Research and Development, Mahidol University, Salaya, Nakhonpathom 73170, Thailand. grbcs@mahidol.ac.thNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

18805449

Citation

Chetsawang, Banthit, et al. "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." Neurochemistry International, vol. 53, no. 6-8, 2008, pp. 283-8.
Chetsawang B, Kooncumchoo P, Govitrapong P, et al. 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. Neurochem Int. 2008;53(6-8):283-8.
Chetsawang, B., Kooncumchoo, P., Govitrapong, P., & Ebadi, M. (2008). 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. Neurochemistry International, 53(6-8), 283-8. https://doi.org/10.1016/j.neuint.2008.08.007
Chetsawang B, et al. 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. Neurochem Int. 2008;53(6-8):283-8. PubMed PMID: 18805449.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - 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. AU - Chetsawang,Banthit, AU - Kooncumchoo,Patcharee, AU - Govitrapong,Piyarat, AU - Ebadi,Manuchair, Y1 - 2008/08/30/ PY - 2008/01/24/received PY - 2008/08/05/revised PY - 2008/08/18/accepted PY - 2008/9/23/pubmed PY - 2009/3/10/medline PY - 2008/9/23/entrez SP - 283 EP - 8 JF - Neurochemistry international JO - Neurochem Int VL - 53 IS - 6-8 N2 - 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. SN - 0197-0186 UR - https://www.unboundmedicine.com/medline/citation/18805449/1_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_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0197-0186(08)00130-7 DB - PRIME DP - Unbound Medicine ER -