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Titolo:
DIETARY RESTRICTION MODULATED CARCINOGEN-DNA ADDUCT FORMATION AND THECARCINOGEN-INDUCED DNA STRAND BREAKS
Autore:
CHOU MW; CHEN W; MIKHAILOVA MV; NICHOLS J; WEIS C; JACKSON CD; HART RW; CHUNG KT;
Indirizzi:
NATL CTR TOXICOL RES JEFFERSON AR 72079 UNIV MEMPHIS MEMPHIS TN 38152
Titolo Testata:
Toxicology letters
fascicolo: 1, volume: 92, anno: 1997,
pagine: 21 - 30
SICI:
0378-4274(1997)92:1<21:DRMCAF>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
CALORIC RESTRICTION; METABOLIZING ENZYMES; ONCOGENE EXPRESSION; FISCHER-344 RATS; DIOL EPOXIDES; BENZO)A>PYRENE; 6-NITROCHRYSENE; PROLIFERATION; APOPTOSIS; MOUSE;
Keywords:
DIETARY RESTRICTION; DNA STRAND BREAKS; AFLATOXIN B-1; AFB(1)-DNA ADDUCT; BENZO[ALPYRENE; BENZO[A]PYRENE-DNA ADDUCT;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
36
Recensione:
Indirizzi per estratti:
Citazione:
M.W. Chou et al., "DIETARY RESTRICTION MODULATED CARCINOGEN-DNA ADDUCT FORMATION AND THECARCINOGEN-INDUCED DNA STRAND BREAKS", Toxicology letters, 92(1), 1997, pp. 21-30

Abstract

Dietary restriction (DR) alters the activities of hepatic drug metabolizing enzymes and modulates the formation of carcinogen-DNA adducts in carcinogen treated animals. Our previous results showed that a 40% restriction of diet (60% of ad libitum (AL) food consumption) reduced the hepatic metabolic activation of aflatoxin B-1 (AFB(1)) but increased the activation of benzo[a]-pyrene (BaP) in both rats and mice. In this study, the focus was directed toward the levels of carcinogen-DNA adducts formation and the carcinogen-induced DNA strand breaks in mousekidney and liver DNA. DR significantly inhibited both AFB(1)-DNA adduct formation and AFB(1)-induced DNA strand breaks in kidney DNA of mice that received a single dose of [H-3]AFB(1) (5 mg/kg). The levels of AFB(1)-DNA adduct formation in mouse kidney DNA correlated well with increased AFB(1)-induced DNA strand breaks. The correlation between thelevels of AFB(1)-DNA-adducts formed and DNA strand breaks in kidney DNA of DR-mice was less linear than between its AL-counterpart suggesting that other factors, such as different rates of DNA repair, may be involved. In addition, DR enhanced hepatic BaP- and 6-nitrochrysene (6-NC)-DNA adduct formation in the mice treated with BaP and 6-NC, respectively. The formation of the specific BaP-adduct, anosinyl)-7,8,9-trihydroxy-7,8,9,10-tetrahydro-BaP (N-2-dG-BaP), in mouse liver was proportional to the dose, and was compatible to the BaP-induced DNA strand breaks affected by DR. The enhancement of the total 6-NC-DNA adduct formation in DR-mouse was also in correlation with the increased 6-NC-induced DNA strand breaks. The activity of mouse liver microsomal nitro-reductase increased by 2-fold in response to DR indicating that the nitroreduction may contribute to the increase of the metabolic activationof 6-NC. Our present results indicate that the effect of DR on the carcinogen activation is dependent upon the DR-modulated carcinogen metabolizing enzyme activities. (C) 1997 Elsevier Science Ireland Ltd.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/07/20 alle ore 06:58:18