ANTIMUTAGENICITY OF XANTHOPHYLLS PRESENT IN AZTEC MARIGOLD (TAGETES ERECTA) AGAINST 1-NITROPYRENE

The principal natural food colorants used in modem food manufacture ar e anthocyanins, betalains, carotenoids, chlorophylls, riboflavin and c aramel. Carotenoids (carotenes and xanthophylls) occur naturally in so me foods such as carrots, red tomatoes, butter, cheese, paprika, palm oil, corn kernels, marigold petals, annatto, and red salmon. Carotenoi ds (alpha- or beta-carotene and xanthophylls) are excellent antioxidan ts and inhibit some types of cancers. In the present study, we used th e Salmonella typhimurium tester strain YG1024 in the plate-incorporati on test to examine the antimutagenicity of xanthophylls extracted from Aztec Marigold (Tagetes erecta) on 1-nitropyrene(1-NP) mutagenicity. Further, we investigated the effect of lutein on DNA-repair system of tester strain YG1023, using a preincubation test. The possible mechani sm of lutein on 1-NP mutagenicity was studied by comparing the absorpt ion spectrum of lutein, 1-NP and lutein plus I-NP. In a dose-response curve of I-NP, the mutagenic potency was 4 317 revertants/nmol, and th e dose of 0.06 mu g of 1-NP/plate was chosen for the antimutagenicity studies. Lutein and xanthophylls from Aztec Marigold (pigments for pou ltry and human use) inhibited mutagenicity of 1-NP in a dose-dependent manner. Lutein and the pigments were not toxic to the bacteria at the concentrations tested (0.002, 0.02, 0.2, 2.0 and 10 mu g/plate). The percentages of inhibition of 1-NP mutagenicity were 72%, 92% and 66.2% for lutein (10 mu g/plate), pigment for poultry use (10 mu g/plate) a nd pigment for human use (7 mu g/plate), respectively. Lutein had no e ffect on the DNA-repair system of strain YG1024. A new peak was detect ed at 429 nm when lutein was added at 1-NP, and it was stable througho ut the incubation time. The results suggest that the major mechanisms of lutein against I-NP mutagenicity is the potential formation of a co mplex between lutein and I-NP, which could limit the bioavailability o f I-NP.