Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Amiodarone induces cytochrome c release and apoptosis through an iodine-independent mechanism
Autore:
Di Matola, T; DAscoli, F; Fenzi, G; Rossi, G; Martino, E; Bogazzi, F; Vitale, M;
Indirizzi:
Univ Naples Federico II, Dipartimento Biol & Patol Cellulare & Mol, I-80131 Naples, Italy Univ Naples Federico II Naples Italy I-80131 Mol, I-80131 Naples, Italy Univ Naples Federico II, Dipartimento Endocrinol & Oncol Mol & Clin, I-80131 Naples, Italy Univ Naples Federico II Naples Italy I-80131 Clin, I-80131 Naples, Italy CNR, Ctr Endocrinol & Oncol Sperimentale G Salvatore, I-56100 Pisa, Italy CNR Pisa Italy I-56100 col Sperimentale G Salvatore, I-56100 Pisa, Italy Univ Pisa, Dipartimento Endocrinol, I-56100 Pisa, Italy Univ Pisa Pisa Italy I-56100 ipartimento Endocrinol, I-56100 Pisa, Italy
Titolo Testata:
JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM
fascicolo: 11, volume: 85, anno: 2000,
pagine: 4323 - 4330
SICI:
0021-972X(200011)85:11<4323:AICCRA>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
FAS-MEDIATED APOPTOSIS; INDUCED THYROTOXICOSIS; THYROID-FUNCTION; ACTIVATION; CELLS; DRUG; PROTEASES; PROTEIN; PHARMACOKINETICS; MITOCHONDRIA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
47
Recensione:
Indirizzi per estratti:
Indirizzo: Vitale, M Univ Naples Federico II, Dipartimento Biol & Patol Cellulare & Mol, Via S Pansini 5, I-80131 Naples, Italy Univ Naples Federico II Via S Pansini 5 Naples Italy I-80131 ly
Citazione:
T. Di Matola et al., "Amiodarone induces cytochrome c release and apoptosis through an iodine-independent mechanism", J CLIN END, 85(11), 2000, pp. 4323-4330

Abstract

Amiodarone (AMD) is one of the most effective antiarrhythmic drugs available. However, its use is often limited by side-effects, mainly hypo- or hyperthyroidism. As AMD displays direct toxic effect on different cell types, we investigated the cytotoxic effect of AMD and its main metabolite, desethylamiodarone (DEA), in thyroid (TAD-2) and nonthyroid (HeLa) cell lines. Both AMD and DEA displayed a dose-dependent toxicity in TAD-2 and HeLa cells, although DEA was more effective. Both TAD-2 and HeLa cells underwent apoptosis, as evidenced by plasma membrane phosphatidylserine exposure and DNA fragmentation. Inhibition of protein synthesis with cycloheximide and inhibition of endogenous peroxidase activity with propylthiouracil did not affect this AMD- and DEA-induced apoptosis in TAD-2 cells. Western blot analysis did not display variations in the expression of p53, Bcl-2, Bcl-XL, and Bax proteins during the treatment with AMD and DEA. Generation of reactive oxygen species, investigated by flow cytometry with dichlorofluorescein diacetate, did not show the production of free radicals during drug treatment. Furthermore, Western blot analysis of cytosolic and mitochondrial fractions prepared from AMD-treated cells demonstrated that AMD induces the release of cytochrome c into the cytosol from the mitochondria. These data indicate that AMD induces cytochrome c release from mitochondria, triggering apoptosis through an iodine-independent mechanism, and that this process is not mediated by modulation of p53, Bcl-2, Bcl-XL, or Bax protein expression and does not involve the generation of free radicals.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 10/07/20 alle ore 09:09:41