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Differential involvement of mitochondrial permeability transition in cytotoxicity of 1-methyl-4-phenylpyridinium and 6-hydroxydopamine.
Mol Cell Biochem. 2006 Sep; 289(1-2):193-200.MC

Abstract

Defects in mitochondrial function have been shown to participate in the induction of neuronal cell injury. The aim of the present study was to assess the influence of the mitochondrial membrane permeability transition inhibition against the toxicity of 1-methyl-4-phenylpyridinium (MPP(+)) and 6-hydroxydopamine (6-OHDA) in relation to the mitochondria-mediated cell death process and role of oxidative stress. Both MPP(+) and 6-OHDA induced the nuclear damage, the changes in the mitochondrial membrane permeability, leading to the cytochrome c release and caspase-3 activation, the formation of reactive oxygen species and the depletion of GSH in differentiated PC12 cells. Cyclosporin A (CsA), trifluoperazine and aristolochic acid, inhibitors of mitochondrial permeability transition, significantly attenuated the MPP(+)-induced mitochondrial damage leading to caspase-3 activation, increased oxidative stress and cell death. In contrast to MPP(+), the cytotoxicity of 6-OHDA was not reduced by the addition of the mitochondrial permeability transition inhibitors. The results show that the cytotoxicity of MPP(+) may be mediated by the mitochondrial permeability transition formation, which is associated with formation of reactive oxygen species and the depletion of GSH. In contrast, the 6-OHDA-induced cell injury appears to be mediated by increased oxidative stress without intervention of the mitochondrial membrane permeability transition.

Authors+Show Affiliations

Department of Pharmacology, College of Medicine, Chung-Ang University, Seoul 156-756, South Korea. leecs@cau.ac.krNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

16625421

Citation

Lee, Chung Soo, et al. "Differential Involvement of Mitochondrial Permeability Transition in Cytotoxicity of 1-methyl-4-phenylpyridinium and 6-hydroxydopamine." Molecular and Cellular Biochemistry, vol. 289, no. 1-2, 2006, pp. 193-200.
Lee CS, Park WJ, Ko HH, et al. Differential involvement of mitochondrial permeability transition in cytotoxicity of 1-methyl-4-phenylpyridinium and 6-hydroxydopamine. Mol Cell Biochem. 2006;289(1-2):193-200.
Lee, C. S., Park, W. J., Ko, H. H., & Han, E. S. (2006). Differential involvement of mitochondrial permeability transition in cytotoxicity of 1-methyl-4-phenylpyridinium and 6-hydroxydopamine. Molecular and Cellular Biochemistry, 289(1-2), 193-200.
Lee CS, et al. Differential Involvement of Mitochondrial Permeability Transition in Cytotoxicity of 1-methyl-4-phenylpyridinium and 6-hydroxydopamine. Mol Cell Biochem. 2006;289(1-2):193-200. PubMed PMID: 16625421.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Differential involvement of mitochondrial permeability transition in cytotoxicity of 1-methyl-4-phenylpyridinium and 6-hydroxydopamine. AU - Lee,Chung Soo, AU - Park,Woo Jae, AU - Ko,Hyun Hee, AU - Han,Eun Sook, Y1 - 2006/04/20/ PY - 2005/12/04/received PY - 2006/02/21/accepted PY - 2006/4/21/pubmed PY - 2006/12/9/medline PY - 2006/4/21/entrez SP - 193 EP - 200 JF - Molecular and cellular biochemistry JO - Mol Cell Biochem VL - 289 IS - 1-2 N2 - Defects in mitochondrial function have been shown to participate in the induction of neuronal cell injury. The aim of the present study was to assess the influence of the mitochondrial membrane permeability transition inhibition against the toxicity of 1-methyl-4-phenylpyridinium (MPP(+)) and 6-hydroxydopamine (6-OHDA) in relation to the mitochondria-mediated cell death process and role of oxidative stress. Both MPP(+) and 6-OHDA induced the nuclear damage, the changes in the mitochondrial membrane permeability, leading to the cytochrome c release and caspase-3 activation, the formation of reactive oxygen species and the depletion of GSH in differentiated PC12 cells. Cyclosporin A (CsA), trifluoperazine and aristolochic acid, inhibitors of mitochondrial permeability transition, significantly attenuated the MPP(+)-induced mitochondrial damage leading to caspase-3 activation, increased oxidative stress and cell death. In contrast to MPP(+), the cytotoxicity of 6-OHDA was not reduced by the addition of the mitochondrial permeability transition inhibitors. The results show that the cytotoxicity of MPP(+) may be mediated by the mitochondrial permeability transition formation, which is associated with formation of reactive oxygen species and the depletion of GSH. In contrast, the 6-OHDA-induced cell injury appears to be mediated by increased oxidative stress without intervention of the mitochondrial membrane permeability transition. SN - 0300-8177 UR - https://www.unboundmedicine.com/medline/citation/16625421/Differential_involvement_of_mitochondrial_permeability_transition_in_cytotoxicity_of_1_methyl_4_phenylpyridinium_and_6_hydroxydopamine_ L2 - https://doi.org/10.1007/s11010-006-9164-0 DB - PRIME DP - Unbound Medicine ER -