Econazole attenuates cytotoxicity of 1-methyl-4-phenylpyridinium by suppressing mitochondrial membrane permeability transition
- Authors
- Lee, Chung Soo; Yim, Soo Bin; Song, Jin Ho; Han, Eun Sook
- Issue Date
- May-2006
- Publisher
- PERGAMON-ELSEVIER SCIENCE LTD
- Keywords
- 1-methyl-4-phenylpyridinium; econazole; PC12 cells; mitochondrial membrane permeability; cell injury
- Citation
- BRAIN RESEARCH BULLETIN, v.69, no.6, pp 687 - 694
- Pages
- 8
- Journal Title
- BRAIN RESEARCH BULLETIN
- Volume
- 69
- Number
- 6
- Start Page
- 687
- End Page
- 694
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/24348
- DOI
- 10.1016/j.brainresbull.2006.03.021
- ISSN
- 0361-9230
1873-2747
- Abstract
- Defects in mitochondrial function have been shown to participate in the induction of neuronal cell injury. The effect of econazole against the cytotoxicity of 1-methyl-4-phenylpyridinium (MPP+) in differentiated PC12 cells was assessed in relation to the mitochondrial membrane permeability changes. Treatment of PC12 cells with MPP+ resulted in the nuclear damage, decrease in the mitochondrial transmembrane potential, cytosolic accumulation of cytochrome c, activation of caspase-3, increase in the formation of reactive oxygen species (ROS) and depletion of GSH. Econazole (0.25-2.5 mu M) inhibited the cytotoxicity of MPP+ or rotenone. The addition of econazole (0.5 mu M) significantly attenuated the MPP+-induced mitochondrial damage, elevation of intracellular Ca2+ level and cell death. However, because of the cytotoxicity, econazole at 5 mu M did not attenuate the toxicity of MPP+. The results show that econazole at the low concentrations may reduce the MPP+-induced viability loss in PC12 cells by suppressing the mitochondrial permeability transition, leading to activation of caspase-3 and the elevation of intracellular Ca2+ levels, which are associated with the increased formation of ROS and depletion of GSH. (c) 2006 Elsevier Inc. All rights reserved.
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