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Titolo:
Cycloheximide and 4-OH-TEMPO suppress chloramphenicol-induced apoptosis inRL-34 cells via the suppression of the formation of megamitochondria
Autore:
Karbowski, M; Kurono, C; Wozniak, M; Ostrowski, M; Teranishi, M; Soji, T; Wakabayashi, T;
Indirizzi:
Nagoya4668550,ch Med, Dept Cell Biol & Mol Pathol, Showa Ku, Nagoya, AichiNagoya Univ Nagoya Aichi Japan 4668550 ol Pathol, Showa Ku, Nagoya, Aichi Nagoya City Univ, Sch Med, Dept Anat, Nagoya, Aichi 4678601, Japan Nagoya City Univ Nagoya Aichi Japan 4678601 Nagoya, Aichi 4678601, Japan Med Univ Gdansk, Dept Biochem, Gdansk, Poland Med Univ Gdansk Gdansk Poland Univ Gdansk, Dept Biochem, Gdansk, Poland
Titolo Testata:
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
fascicolo: 1, volume: 1449, anno: 1999,
pagine: 25 - 40
SICI:
0167-4889(19990204)1449:1<25:CA4SCA>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
HYDRAZINE-INDUCED FORMATION; ELECTRON-TRANSPORT CHAIN; STRESS-INDUCED APOPTOSIS; RAT-LIVER STRUCTURE; OXIDATIVE STRESS; PHYSICOCHEMICAL PROPERTIES; MITOCHONDRIAL-MEMBRANES; THYMOCYTE APOPTOSIS; BIOCHEMICAL-PROPERTIES; SUPEROXIDE-DISMUTASE;
Keywords:
cycloheximide; apoptosis; TEMPO; RL-34 cell; megamitochondria;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
73
Recensione:
Indirizzi per estratti:
Indirizzo: Wakabayashi, T Nagoyao,niv, Sch Med, Dept Cell Biol & Mol Pathol, Showa Ku, 65 Tsurumai Ch Nagoya Univ 65 Tsurumai Cho Nagoya Aichi Japan 4668550 i Ch
Citazione:
M. Karbowski et al., "Cycloheximide and 4-OH-TEMPO suppress chloramphenicol-induced apoptosis inRL-34 cells via the suppression of the formation of megamitochondria", BBA-MOL CEL, 1449(1), 1999, pp. 25-40

Abstract

Toxic effects of chloramphenicol, an antibiotic inhibitor of mitochondrialprotein synthesis, on rat liver derived RL-34 cell line were completely blocked by a combined treatment with substances endowed with direct or indirect antioxidant properties. A stable, nitroxide free radical scavenger, 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl, and a protein synthesis inhibitor, cycloheximide, suppressed in a similar manner the following manifestations of the chloramphenicol cytotoxicity: (1) Oxidative stress state as evidenced by FAGS analysis of cells loaded with carboxy-dichlorodihydrofluorescein diacetate and Mite Tracker CMTH(2)MRos; (2) megamitochondria formation detected by staining of mitochondria with MitoTracker CMXRos under a laser confocal microscopy and electron microscopy; (3) apoptotic changes of the cell detected by the phase contrast microscopy, DNA laddering analysis and cell cycle analysis. Since increases of ROS generation in chloramphenicol-treated cells were the first sign of the chloramphenicol toxicity, we assume that oxidative stress state is a mediator of above described alternations of RL-34 cells including MG formation. Pretreatment of cells with cycloheximide or 4-hydroxy-2,2,6, 6-tetramethylpiperidine-1-oxyl, which is known to be localized into mitochondria, inhibited the megamitochondria formation andsucceeding apoptotic changes of the cell. Protective effects of cycloheximide, which enhances the expression of Bcl-2 protein, may further confirm our hypothesis that the megamitochondria formation is a cellular response to an increased ROS generation and raise a possibility that antiapoptotic action of the drug is exerted via the protection of the mitochondria functions. (C) 1999 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/01/20 alle ore 12:21:36