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Titolo:
Cytogenetic effects of propyl gallate in CHO-K1 cells
Autore:
Tayama, S; Nakagawa, Y;
Indirizzi:
Tokyo Metropolitan Res Lab Publ Hlth, Dept Toxicol, Shinjuku Ku, Tokyo 1690073, Japan Tokyo Metropolitan Res Lab Publ Hlth Tokyo Japan 1690073 1690073, Japan
Titolo Testata:
MUTATION RESEARCH-GENETIC TOXICOLOGY AND ENVIRONMENTAL MUTAGENESIS
fascicolo: 1-2, volume: 498, anno: 2001,
pagine: 117 - 127
SICI:
1383-5718(20011115)498:1-2<117:CEOPGI>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
SISTER-CHROMATID EXCHANGES; HYDROGEN-PEROXIDE; PROTECTIVE ROLE; CYTOTOXICITY; MUTAGENICITY; INDUCTION; PHENYLPHENOL; CARCINOGENS; METABOLITE; DAMAGE;
Keywords:
propyl gallate; gallic acid; ellagic acid; rat liver S9; sister-chromatid exchange; chromosomal aberration; CHO-K1 cell; HPLC analysis;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
33
Recensione:
Indirizzi per estratti:
Indirizzo: Tayama, S Tokyo Metropolitan Res Lab Publ Hlth, Dept Toxicol, Shinjuku Ku,3-24-1 Hyakunincho, Tokyo 1690073, Japan Tokyo Metropolitan Res Lab Publ Hlth 3-24-1 Hyakunincho Tokyo Japan 1690073
Citazione:
S. Tayama e Y. Nakagawa, "Cytogenetic effects of propyl gallate in CHO-K1 cells", MUT RES-GTE, 498(1-2), 2001, pp. 117-127

Abstract

We investigated whether propyl gallate (PG) can induce sister-chromatid exchanges (SCEs) and chromosomal aberrations (CAs) in CHO-K I cells. In the absence of an exogeneous metabolizing system, treatments with 0.25-1.5 mM PGin plugged flasks for 3 It resulted in increases in SCEs, CAs, and endoreduplications (ERDs), which were followed by an increase in the percentage ofcells showing cell-cycle delay. At the end of the treatment, a decrease inPG concentration and production of PG dimer and ellagic acid (EA) in the medium were detected, indicating that PG had autoxidized. EA, an oxide of PG, was not genotoxic even at 0.3 mM, the maximum concentration soluble in the medium. Several oxygen radical scavengers (superoxide dismutase (SOD), catalase, glutathione and o-phenanthroline (OP)) and an inhibitor of catalaseactivity (3-amino-1,2,4-triazole (AT)), did not significantly influence PGgenotoxicity. When PG autoxidation was suppressed by low pH (6.8) or a 5% CO2 atmosphere, cell-cycle delay intensified and induction of SCEs and CAs occurred even at the lowest PG dose (0.1 mM). When PG (0.5 mM) was assayed in the presence of S9 (1.5-9%), gallic acid (GA), a metabolite of PG, was generated in direct proportion to the S9 concentration, while cell-cycle delay and genotoxic effects varied inversely with S9 concentration at the levels over 3%. GA also autoxidized and at greater than or equal to 0.5 mM it induced SCEs. Both catalase and AT suppressed the induction of SCEs by GA orinhibited cell proliferation, indicating that H2O2 participated in the effects. In conclusion, PG in the presence or absence of S9 can induce SCEs, CAs, and ERDs, and the oxides, metabolites and oxygen-free radicals generated during the treatment are partly responsible for these effects. (C) 2001 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 31/03/20 alle ore 21:33:53