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Titolo:
MUTAGENICITY OF METABOLIC OXYGEN RADICALS IN MAMMALIAN-CELL CULTURES
Autore:
GILLE JJP; VANBERKEL CGM; JOENJE H;
Indirizzi:
FREE UNIV AMSTERDAM,DEPT HUMAN GENET,DEPT MED ONCOL,VAN DERBOECHORSTSTR 7 1081 BT AMSTERDAM NETHERLANDS
Titolo Testata:
Carcinogenesis
fascicolo: 12, volume: 15, anno: 1994,
pagine: 2695 - 2699
SICI:
0143-3334(1994)15:12<2695:MOMORI>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
HAMSTER OVARY CELLS; HETEROZYGOUS AUTOSOMAL LOCUS; INDUCED CHROMOSOMAL BREAKAGE; DIPLOID HUMAN-LYMPHOBLASTS; BLOOMS SYNDROME; NORMOBARIC HYPEROXIA; HYDROGEN-PEROXIDE; OXIDATIVE STRESS; MUTATIONS; RECOMBINATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
32
Recensione:
Indirizzi per estratti:
Citazione:
J.J.P. Gille et al., "MUTAGENICITY OF METABOLIC OXYGEN RADICALS IN MAMMALIAN-CELL CULTURES", Carcinogenesis, 15(12), 1994, pp. 2695-2699

Abstract

Reactive oxygen species produced by normal cellular metabolism have been considered to play a causative role in spontaneously occurring genomic instability and carcinogenesis, To study the genotoxic consequences of an enhanced flux of metabolically produced reactive oxygen species, cells may be exposed to hyperoxia (elevated concentrations of oxygen), a condition known tea generate high levels of microscopically visible chromosomal damage. Here we assess the mutagenic potential of normobaric hyperoxia in several mammalian cells lines (CHO-K1-BH4 and AS52 Chinese hamster cells and TK6 human lymphoblastoid cells) using different target genes, including hprt, xprt and tk. Exposure of cell cultures to hyperoxia to 10-40% clonogenic cell survival, failed to inducemutations at the hprt and xprt loci, In human TK6 cells, hyperoxia failed to induce normal growing tk mutants, but efficiently induced slowgrowing tk mutants, The latter type of mutant is supposed to result from very large deletions or multilocus events, Our results suggest that elevated levels of endogenous activated oxygen species are inefficient in inducing point mutations or small deletions, but tend to generate gross rearrangements, Mammalian cells under oxidative stress thus exhibit a hyper-recombination phenotype, The carcinogenic impact of metabolic oxygen radical fluxes may thus be based on enhanced mitotic recombination rates, leading to tumor suppressor gene inactivation through'loss of heterozygosity'.

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Documento generato il 29/03/20 alle ore 09:16:04