Tags

Type your tag names separated by a space and hit enter

Modulation of 1-methyl-4-phenylpyridinium-induced mitochondrial dysfunction and cell death in PC12 cells by K(ATP) channel block.
J Neural Transm (Vienna). 2007 Mar; 114(3):297-305.JN

Abstract

The present study investigated the effect of 5-hydroxydecanoate, a selective mitochondrial K(ATP) channel blocker, on the cytotoxicity of neurotoxin 1-methyl-4-phenylpyridinium (MPP(+)) in differentiated PC12 cells. 5-Hydroxydecanoate and glibenclamide (a cell surface and mitochondrial K(ATP) channel inhibitor) reduced the MPP(+)-induced cell death and GSH depletion and showed a maximal inhibitory effect at 5 and 10 microM, respectively. Addition of 5-hydroxydecanoate attenuated the MPP(+)-induced nuclear damage, changes in the mitochondrial membrane permeability and increase in the reactive oxygen species formation in PC12 cells. The results show that 5-hydroxydecanote may prevent the MPP(+)-induced viability loss in PC12 cells by suppressing formation of the mitochondrial permeability transition, leading to the cytochrome c release and caspase-3 activation. This effect appears to be accomplished by the inhibitory action on the formation of reactive oxygen species and the depletion of GSH. The blockade of mitochondrial K(ATP) channels seems to prevent the MPP(+)-induced neuronal cell damage.

Authors+Show Affiliations

Department of Pharmacology, College of Medicine, Chung-Ang University, Seoul, South Korea. leecs@cau.ac.ukNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

17109075

Citation

Lee, C S., et al. "Modulation of 1-methyl-4-phenylpyridinium-induced Mitochondrial Dysfunction and Cell Death in PC12 Cells By K(ATP) Channel Block." Journal of Neural Transmission (Vienna, Austria : 1996), vol. 114, no. 3, 2007, pp. 297-305.
Lee CS, Kim YJ, Ko HH, et al. Modulation of 1-methyl-4-phenylpyridinium-induced mitochondrial dysfunction and cell death in PC12 cells by K(ATP) channel block. J Neural Transm (Vienna). 2007;114(3):297-305.
Lee, C. S., Kim, Y. J., Ko, H. H., & Han, E. S. (2007). Modulation of 1-methyl-4-phenylpyridinium-induced mitochondrial dysfunction and cell death in PC12 cells by K(ATP) channel block. Journal of Neural Transmission (Vienna, Austria : 1996), 114(3), 297-305.
Lee CS, et al. Modulation of 1-methyl-4-phenylpyridinium-induced Mitochondrial Dysfunction and Cell Death in PC12 Cells By K(ATP) Channel Block. J Neural Transm (Vienna). 2007;114(3):297-305. PubMed PMID: 17109075.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Modulation of 1-methyl-4-phenylpyridinium-induced mitochondrial dysfunction and cell death in PC12 cells by K(ATP) channel block. AU - Lee,C S, AU - Kim,Y J, AU - Ko,H H, AU - Han,E S, Y1 - 2006/11/17/ PY - 2006/03/05/received PY - 2006/10/03/accepted PY - 2006/11/17/pubmed PY - 2007/6/22/medline PY - 2006/11/17/entrez SP - 297 EP - 305 JF - Journal of neural transmission (Vienna, Austria : 1996) JO - J Neural Transm (Vienna) VL - 114 IS - 3 N2 - The present study investigated the effect of 5-hydroxydecanoate, a selective mitochondrial K(ATP) channel blocker, on the cytotoxicity of neurotoxin 1-methyl-4-phenylpyridinium (MPP(+)) in differentiated PC12 cells. 5-Hydroxydecanoate and glibenclamide (a cell surface and mitochondrial K(ATP) channel inhibitor) reduced the MPP(+)-induced cell death and GSH depletion and showed a maximal inhibitory effect at 5 and 10 microM, respectively. Addition of 5-hydroxydecanoate attenuated the MPP(+)-induced nuclear damage, changes in the mitochondrial membrane permeability and increase in the reactive oxygen species formation in PC12 cells. The results show that 5-hydroxydecanote may prevent the MPP(+)-induced viability loss in PC12 cells by suppressing formation of the mitochondrial permeability transition, leading to the cytochrome c release and caspase-3 activation. This effect appears to be accomplished by the inhibitory action on the formation of reactive oxygen species and the depletion of GSH. The blockade of mitochondrial K(ATP) channels seems to prevent the MPP(+)-induced neuronal cell damage. SN - 0300-9564 UR - https://www.unboundmedicine.com/medline/citation/17109075/Modulation_of_1_methyl_4_phenylpyridinium_induced_mitochondrial_dysfunction_and_cell_death_in_PC12_cells_by_K_ATP__channel_block_ L2 - https://doi.org/10.1007/s00702-006-0594-3 DB - PRIME DP - Unbound Medicine ER -