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Titolo:
ASCORBIC-ACID (VITAMIN-C) MODULATES THE MUTAGENIC EFFECTS PRODUCED BYAN ALKYLATING AGENT IN-VIVO
Autore:
AIDOO A; LYNCOOK LE; LENSING S; WAMER W;
Indirizzi:
US FDA,NATL CTR TOXICOL RES,DEPT HLTH & HUMAN SERV,DIV GENET TOXICOL,HTF 120,3900 NCTR RD JEFFERSON AR 72079 COMP BASED SYST INC JEFFERSON AR 00000 US FDA,CTR FOOD & NUTR SAFETY WASHINGTON DC 20204
Titolo Testata:
Environmental and molecular mutagenesis
fascicolo: 3, volume: 24, anno: 1994,
pagine: 220 - 228
SICI:
0893-6692(1994)24:3<220:A(MTME>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
ETHYL-N-NITROSOUREA; BETA-CAROTENE; CHROMOSOMAL-ABERRATIONS; SALMONELLA-TYPHIMURIUM; CELL-PROLIFERATION; FISCHER-344 RATS; COVALENT BINDING; BONE-MARROW; LYMPHOCYTES; INHIBITION;
Keywords:
ASCORBIC ACID; ANTIMUTAGENICITY; N-ETHYL-N-NITROSOUREA; SPLEEN AND THYMUS LYMPHOCYTES;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
51
Recensione:
Indirizzi per estratti:
Citazione:
A. Aidoo et al., "ASCORBIC-ACID (VITAMIN-C) MODULATES THE MUTAGENIC EFFECTS PRODUCED BYAN ALKYLATING AGENT IN-VIVO", Environmental and molecular mutagenesis, 24(3), 1994, pp. 220-228

Abstract

Recent reports suggest that ascorbic acid (vitamin C) inhibits tumorigenesis as well as exerts a protective effect against mutagenesis in vitro; however, there is no information on its ability to affect gene mutations induced in vivo. In this study, we have investigated the antimutagenic effects of ascorbic acid on the frequency of 6-thioguanine-resistant (6-TG(r)) T-lymphocytes produced in Fischer 344 rats dosed with the direct-acting alkylating agent, N-ethyl-N-nitrosourea (ENU). The frequency of 6-TG(r) T-lymphocytes from the spleen measured five weeks after ENU treatment indicated that ENU produced a substantial mutagenic response. Pretreatment and/or post-treatment of mts with ascorbicacid administered in the drinking water appeared to inhibit the response, but the inhibition was statistically significant only when data from the various dosing schedules were pooled. In addition, there was no clear dose-dependency to the inhibitory effect of ascorbic acid. To further evaluate the time effects of the vitamin supplement on ENU mutagenicity, rats were exposed to the mutagen together with ascorbic acid, which was given continuously for the entire duration of the experiment. At specific times after ENU treatment, the frequency of 6-TG(r) T-cells was determined in lymphocytes isolated from the spleen and the thymus. Time-dependent increases in the frequency of 6-TG(r) T-cells were observed with ENU treatment; ascorbic acid significantly reduced the ENU-mediated mutagenic responses, most dramatically in the spleen at weeks 6 and 8 (P < 0.0001), and to a lesser extent in the thymus (P < 0.01 at week 6 and P < 0.006 at week 8). Our data suggest that ascorbic acid intake affects the in vivo mutagenicity of ENU, a direct-acting mutagen/carcinogen, and that the reported inhibitory effects of theantioxidant on carcinogenesis may be partially mediated by its effects on mutagenesis. Although it is difficult to extrapolate from rodent studies to humans, the results presented suggest an explanation for epidemiological data that link vitamin C ingestion with decreased cancerrisk. (C) 1994 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 07/07/20 alle ore 22:34:04