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Effect of annatto on micronuclei induction by direct and indirect mutagens in HepG2 cells
Author(s) -
Barcelos Gustavo Rafael Mazzaron,
Angeli José Pedro Friedmann,
Serpeloni Juliana Mara,
Rocha Bruno Alves,
Mantovani Mário Sérgio,
Antunes Lusânia Maria Greggi
Publication year - 2009
Publication title -
environmental and molecular mutagenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 87
eISSN - 1098-2280
pISSN - 0893-6692
DOI - 10.1002/em.20494
Subject(s) - mutagen , micronucleus test , antimutagen , methyl methanesulfonate , micronucleus , chemistry , antioxidant , cytotoxicity , carcinogen , in vitro , biochemistry , pharmacology , toxicity , biology , dna damage , dna , organic chemistry
Annatto (AN), a natural food colorant rich in carotenoids, has been reported as being an effective antioxidant, but little is known about its potential chemopreventive properties. In this study, we evaluated the ability of AN to protect human hepatoma cells (HepG2) from micronucleus (MN) induction against three different mutagens: benzo(a)pyrene (B(a)P), doxorubicin (DXR), and methyl methanesulfonate (MMS). In an attempt to clarify the possible mechanism of antimutagenicity of AN, three protocols of treatment were applied (pretreatment; simultaneous treatment, and post‐treatment with AN following treatment with the mutagens). Also, cells exposed only to AN were assayed for cytotoxicity and mutagenicity. A dosage up to 10 μg/ml of AN was devoid of mutagenic activity. Protective effects were seen on micronuclei induced by B(a)P and DXR using pre and simultaneous treatment, but AN had no significant effect on MN induction by MMS in any of the protocols. Our results also show that exposure of cells to concentrations of AN higher than 10 μg/ml decreased cell viability. Taken together, our findings indicate that AN presents antimutagenic activity in vitro, but its protective effect is dependent on the mutagen and on type of treatment suggesting its potential use as a chemopreventive agent. Environ. Mol. Mutagen. 2009. © 2009 Wiley‐Liss, Inc.