INHIBITORY EFFECTS OF ELLAGIC ACID ON THE DIRECT-ACTING MUTAGENICITY OF AFLATOXIN B-1 IN THE SALMONELLA MICROSUSPENSION ASSAY

Citation
G. Loarcapina et al., INHIBITORY EFFECTS OF ELLAGIC ACID ON THE DIRECT-ACTING MUTAGENICITY OF AFLATOXIN B-1 IN THE SALMONELLA MICROSUSPENSION ASSAY, Mutation research. Fundamental and molecular mechanisms of mutagenesis, 398(1-2), 1998, pp. 183-187
Citations number
23
Categorie Soggetti
Genetics & Heredity",Toxicology,"Biothechnology & Applied Migrobiology
Journal title
Mutation research. Fundamental and molecular mechanisms of mutagenesis
ISSN journal
13861964 → ACNP
Volume
398
Issue
1-2
Year of publication
1998
Pages
183 - 187
Database
ISI
SICI code
1386-1964(1998)398:1-2<183:IEOEAO>2.0.ZU;2-0
Abstract
Ellagic acid (EA) is a phenolic compound that exhibits both antimutage nic and anticarcinogenic activity in a wide range of assays-in vitro a nd in vivo. It occurs naturally in some foods such as strawberries, ra spberries, and grapes. In the previous work, we used the Salmonella mi crosuspension assay to examine the antimutagenicity of EA against the potent mutagen aflatoxin B-1 (AFB(1)) using tester strains TA98 and TA 100. Briefly, the microsuspension assay was approximately 10 times mor e sensitive than the standard Salmonella/microsome (Ames) test in dete cting AFB(1) mutagenicity, and EA significantly inhibited mutagenicity of all AFB(1) doses in both tester strains with the addition of S9. T he greatest inhibitory effect of EA on AFB(1) mutagenicity occurred wh en EA and AFB(1) were incubated together (with metabolic enzymes). Low er inhibition was apparent when the cells were first incubated with EA followed by a second incubation with AFB(1), or when the cells were f irst incubated with AFB(1) followed by a second incubation with EA alo ne, all with metabolic enzymes. The result of these sequential incubat ion studies indicates that one mechanism of inhibition could involve t he formation of an AFB(1)-EA chemical complex. In the present study, w e further examine the effect of EA on AFB(1) mutagenicity, but without the addition of exogenous metabolic enzymes. We report the mutagenici ty of AFB(1) in the microsuspension assay using TA98 and TA100 without the addition of S9. Neither the concentrations of AFB(1) (0.6, 1.2, a nd 2.4 mu g/tube) nor the concentrations of EA (0.3, 1.5, 3, 10, and 2 0 mu g/tube) were toxic to the bacteria. The results indicate that AFB (1) is a direct-acting mutagen, and that EA inhibits AFB(1) direct-act ing mutagenicity. (C) 1998 Elsevier Science B.V.