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Titolo:
A ROLE FOR APOPTOSIS IN THE TOXICITY AND MUTAGENICITY OF BLEOMYCIN INAHH-1 TK(+ -) HUMAN LYMPHOBLASTOID-CELLS/
Autore:
MORRIS SM; DOMON OE; MCGARRITY LJ; CHEN JJ; MANJANATHA MG; ANDREWS AM; AIDOO A; CASCIANO DA;
Indirizzi:
NATL CTR TOXICOL RES,DIV GENET TOXICOL,HFT 120,3900 NCTR RD JEFFERSONAR 72079 US FDA,NATL CTR TOXICOL RES,DIV GENET TOXICOL,DEPT HLTH & HUMAN SERV JEFFERSON AR 72079 US FDA,NATL CTR TOXICOL RES,DIV BIOMETRY & RISK ASSESSMENT,DEPT HLTH & HUMAN SERV JEFFERSON AR 72079 PATHOL ASSOC INT JEFFERSON AR 72079
Titolo Testata:
Mutation research
fascicolo: 1-2, volume: 357, anno: 1996,
pagine: 143 - 165
SICI:
0027-5107(1996)357:1-2<143:ARFAIT>2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
CHEMOTHERAPY-INDUCED APOPTOSIS; RADIATION-INDUCED APOPTOSIS; DOUBLE-STRAND CLEAVAGE; ASCITES TUMOR-CELLS; BCL-2 GENE FAMILY; P53 STATUS; 6-THIOGUANINE-RESISTANT MUTANTS; SUPEROXIDE-DISMUTASE; MUTATION-INDUCTION; ANTICANCER AGENTS;
Keywords:
BLEOMYCIN; APOPTOSIS; CYTOTOXICITY; TK MUTATION; HPRT MUTATION; HUMAN LYMPHOBLASTOID CELL;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
76
Recensione:
Indirizzi per estratti:
Citazione:
S.M. Morris et al., "A ROLE FOR APOPTOSIS IN THE TOXICITY AND MUTAGENICITY OF BLEOMYCIN INAHH-1 TK(+ -) HUMAN LYMPHOBLASTOID-CELLS/", Mutation research, 357(1-2), 1996, pp. 143-165

Abstract

The chromosomal mutagen, bleomycin, is also noted for its toxic properties, although the mechanism of cell death is not fully understood. In order to determine if cell death occurred by apoptosis or necrosis, AHH-1 tk(+/-) cells were exposed to bleomycin and the percentage of viable, apoptotic and necrotic cells quantified by flow cytometry. Logistic regression analysis indicated that the primary manner of cell death was through the apoptosis pathways, that apoptosis was delayed, and that apoptosis was accompanied by an arrest in the G(2) phase of the cell cycle, Once apoptosis was established as a mechanism for cell death, the efficiency with which these pathways removed damaged cells fromthe population was evaluated with the use of specific-locus mutation assays (tk and hprt) as indicators of cells with DNA damage that maintained viability and clonogenicity. Linear regression analysis detecteda significant, concentration-dependent increase in the numbers of TFTr clones with the slow-growth phenotype. This suggests that a proportion of cells with bleomycin-induced DNA damage did not undergo cell death by apoptosis and that apoptosis, a mechanism for the destruction ofdamaged cells, is not fully efficient in the AHH-1 tk(+/-) cell line.

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Documento generato il 01/04/20 alle ore 16:44:04