Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Oxidative stress mediates neuronal DNA damage and apoptosis in response tocytosine arabinoside
Autore:
Geller, HM; Cheng, KY; Goldsmith, NK; Romero, AA; Zhang, AL; Morris, EJ; Grandison, L;
Indirizzi:
Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Pharmacol, Piscataway, NJ 08854 USA Univ Med & Dent New Jersey Piscataway NJ USA 08854scataway, NJ 08854 USA Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Physiol & Biophys, Piscataway, NJ 08854 USA Univ Med & Dent New Jersey Piscataway NJ USA 08854 scataway, NJ 08854 USA
Titolo Testata:
JOURNAL OF NEUROCHEMISTRY
fascicolo: 2, volume: 78, anno: 2001,
pagine: 265 - 275
SICI:
0022-3042(200107)78:2<265:OSMNDD>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
CEREBELLAR GRANULE NEURONS; KILLS POSTMITOTIC NEURONS; ARA-C; ANTIOXIDANT ACTIVITY; MOLECULAR PHARMACOLOGY; GLUTATHIONE PEROXIDASE; SIGNAL-TRANSDUCTION; EMBRYONIC NEURONS; MYELOID-LEUKEMIA; POLYMERASE-BETA;
Keywords:
antioxidant; cell death; comet; DNA strand break; flow cytometry; neuroprotection;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
62
Recensione:
Indirizzi per estratti:
Indirizzo: Geller, HM Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Pharmacol, 675 Hoes Lane, Piscataway, NJ 08854 USA Univ Med & Dent New Jersey 675 Hoes Lane Piscataway NJ USA 08854
Citazione:
H.M. Geller et al., "Oxidative stress mediates neuronal DNA damage and apoptosis in response tocytosine arabinoside", J NEUROCHEM, 78(2), 2001, pp. 265-275

Abstract

Cytosine arabinoside (AraC) is a nucleoside analog that produces significant neurotoxicity in cancer patients. The mechanism by which AraC causes neuronal death is a matter of some debate because the conventional understanding of AraC toxicity requires incorporation into newly synthesized DNA. Herewe demonstrate that AraC-induced apoptosis of cultured cerebral cortical neurons is mediated by oxidative stress. AraC-induced cell death was reducedby treatment with several different free-radical scavengers (N-acetyl-L-cysteine, dipyridamole, uric acid, and vitamin E) and was increased followingdepletion of cellular glutathione stores. AraC induced the formation of reactive oxygen species in neurons as measured by an increase in the fluorescence of the dye 5-(6)-carboxy-2 ' ,7 ' -dichlorodihydrofluorescein diacetate. AraC produced DNA single-strand breaks as measured by single-cell gel electrophoresis and the level of DNA strand breakage was reduced by treatmentwith the free radical scavengers. These data support a model in which AraCinduces neuronal apoptosis by provoking the generation of reactive oxygen species, causing oxidative DNA damage and initiating the p53-dependent apoptotic program. These observations suggest the use of antioxidant therapies to reduce neurotoxicity in AraC chemotherapeutic regimens.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/11/20 alle ore 16:16:09