Physicochemical and nutraceutical properties of moringa (Moringa oleifera) leaves and their effects in an in vivo AOM/DSS-induced colorectal carcinogenesis model.

Moringa (Moringa oleifera) is a plant that has generated great interest in recent years because of its attributed medicinal properties. The aim of this study was to characterize the bioactive compounds of moringa leaves (MO) and evaluate their effect on a colorectal carcinogenesis model. Twenty-four male CD-1 mice were divided into 4 groups: Group 1 fed with basal diet (negative control/NC); Group 2 received AOM/DSS (positive control); Groups 3 and 4 were fed with basal diet supplemented with moringa leaves (2.5% w/w and 5% w/w, respectively) for 12weeks. Moringa leaves exhibited a high content of dietary fiber (~18.75%) and insoluble dietary fiber (2.29%). There were identified 9 phenolic compounds whereas the chlorogenic and ρ-coumaric acid showed the higher contents (44.23-63.34µg/g and 180.45-707.42µg/g, respectively). Moringa leaves decreased the activity of harmful fecal enzymes (ß-glucosidase, ß-glucuronidase, tryptophanase and urease up to 40%, 43%, 103% and 266%, respectively) as well tumors incidence in male CD1-mice (~50% with 5% w/v of moringa dose). These findings suggest that the bioactive compounds of moringa such as total dietary fiber and phenolic compounds may have chemopreventive capacity. This is the first study of the suppressive effect of moringa leaves in an in vivo model of AOM/DSS-induced colorectal carcinogenesis.

Dietary supplementation of lutein reduces colon carcinogenesis in DMH-treated rats by modulating K-ras, PKB, and ß-catenin proteins.

In colon cancer, disturbances have been detected in genes coding for proteins involved in cellular proliferation, such as K-ras, ß-catenin, extracellular signal-regulated kinases (ERKs), and the protein kinase B (PKB). Although carotenoids such as lutein have an important role to prevent and treat some types of cancer, there are very few studies about the effect of lutein against colon cancer and its activity at the molecular level. Therefore, the aim of this study was to evaluate the chemoprotective activity of lutein against colon cancer induced by dimethylhydrazine (DMH). The results showed a significant increase in protein expression for K-ras and ß-catenin in tumors of DMH-treated rats. Simultaneously, we detected changes in the phosphorylation state of ERK1/2 and PKB in DMH-treated animals. Lutein given in the diet (0.002%), before (prevention) and after (treatment) DMH administration, diminished the number of tumors by 55% and 32%, respectively. Moreover, lutein significantly decreased in tumors the expression of K-ras (25%) and ß-catenin (28%) and the amount of pPKB (32%), during the prevention, and 39%, 26%, and 26% during the treatment stage, respectively. This study demonstrates the chemoprotective effect of lutein against colon cancer by modulating the proliferative activity of K-ras, PKB, and ß-catenin proteins.

Hibiscus sabdariffa L. extracts inhibit the mutagenicity in microsuspension assay and the proliferation of HeLa cells.

Hibiscus sabdariffa L. is used as a refreshing beverage and as a traditional medicine. The objective of this study was to determine the in vitro effect of phenolic compounds present in aqueous, ethyl acetate, and chloroform extracts of H. sabdariffa against mutagenicity of 1-nitropyrene (1-NP), and also the antiproliferative effect of these extracts. Inhibition of cell proliferation and DNA fragmentation were tested on transformed human HeLa cells. The hot aqueous extract (HAE) contained 22.27 +/- 2.52 mg of protocatechuic acid (PCA) per gram of lyophilized dried extract, and was not statistically different from the cold aqueous or chloroform extracts; the ethyl acetate extract produced the least amount of PCA. The H. sabdariffa extracts inhibited mutagenicity of 1-NP in a dose-response manner. The inhibition rate on HeLa cells of HAE was also dose-dependent. The HAE did not induce DNA fragmentation. The results suggest that H. sabdariffa L. extracts have antimutagenic activity against 1-NP and decrease the proliferation of HeLa cells, probably due to phenolic acid composition.

Antimutagenic activity of phenolic compounds, oligosaccharides and quinolizidinic alkaloids from Lupinus campestris seeds.

There are some foods that contain mutagenic or carcinogenic agents, some of which occur naturally and others that may be formed during preparation or cooking. Several foods such as legumes, also contain natural antimutagens and/or anticarcinogens. Lupine is one such legume that contains high amounts of protein (40%) and oils (14%). About 90 species of lupine have been reported throughout Mexico. However, the use of this crop as a source of food has been limited by the presence of antinutritional agents such as phenolic compounds (PC), carbohydrates (CH) and quinolizidinic alkaloids (Qas). It has also been suggested that consuming these compounds can affect human health and may even reduce the risk of disease. The objective of this work was to determine the effect of PC, CH and Qas, isolated and quantified from Lupinus campestris on the mutagenicity of 1-nitropyrene (1-NP) as a model mutagen and we used the Salmonella typhimurium tester strain YG1024 by the Kado microsuspension method. The results indicate that L. campestris seeds have 11 mg (+)catechin equivalent g(-1) seed coat; 120.3 mg g(-1) seeds and 2.13 mg g(-1) seeds of PC, CH and Qas, respectively. 1-NP mutagenicity was inhibited by 86% for PC, 76% for CH and 75% for Qas at concentrations of 200, 512 and 13.6 microg/tube, respectively.

Comparison of nixtamalization and extrusion processes for a reduction in aflatoxin content.

Traditional nixtamalization and an extrusion method for making the dough (masa) for corn tortillas that requires using lime and hydrogen peroxide were evaluated for the detoxification of aflatoxins. The traditional nixtamalization process reduced levels of aflatoxin B(1) (AFB(1)) by 94%, aflatoxin M(1) (AFM(1)) by 90% and aflatoxin B(1)-8,9-dihydrodiol (AFB(1)-dihydrodiol) by 93%. The extrusion process reduced levels of AFB(1) by 46%, AFM(1) by 20% and AFB(1)-dihydrodiol by 53%. Extrusion treatments with 0, 0.3 and 0.5% lime reduced AFB(1) levels by 46, 74 and 85%, respectively. The inactivation of AFB(1), AFM(1) and AFB(1)-dihydrodiol in the extrusion process using lime together with hydrogen peroxide showed higher elimination of AFB(1) than treatments with lime or hydrogen peroxide alone. The extrusion process with 0.3% lime and 1.5% hydrogen peroxide was the most effective process to detoxify aflatoxins in corn tortillas, but a high level of those reagents negatively affected the taste and aroma of the corn tortilla as compared with tortillas elaborated by the traditional nixtamalization process.

Antimutagenic effects of natural phenolic compounds in beans.

Polyphenols in fruits, vegetables (e.g., flavonols like quercetin) and tea (e.g., catechins such as epigallocatechin gallate) are good antioxidants with antimutagenic and anticarcinogenic properties. In the present study, the Salmonella typhimurium tester strain YG1024 was used in the plate-incorporation test to examine the antimutagenic effect of phenolic compounds, extracted from common beans (Phaseolus vulgaris), on 1-NP and B[a]P mutagenicity. Dose-response curves for 1-NP and B[a]P were obtained; the number of net revertants/plate at the peak mutagenic dosage were 880 for 1-NP and 490 for B[a]P. For the antimutagenicity studies doses of 0.1 microg/plate and 2 microg/plate for 1-NP and B[a]P, respectively, were chosen. We obtained a dose-response curve of ellagic acid (EA) against B[a]P and 1-NP mutagenicity. To test the bean extract, a dose of 300 microg/plate of EA was chosen as the antimutagenic control. The EA and bean extracts were not toxic to the bacteria at the concentrations tested. The inhibitory effects of the bean extracts and EA against B[a]P mutagenicity were dose-dependent. The percentages of inhibition produced against B[a]P (2 microg/plate) using 300 microg/plate of EA and for the extracts 500 microg equivalent catechin/plate were 82%, 83%, 81% and 83% for EA, water extract, water/methanol extract and methanol extract, respectively. However, for 1-NP mutagenicity, only the methanolic extract from beans showed an inhibitory effect. These results suggest that common beans, as other legumes, can function as health-promoting foods.

Antimutagenic activity of carotenoids in green peppers against some nitroarenes.

In Mexico, as well as in Central and South American countries, the consumption of peppers (Capsicum annuum) has been tradition for thousands of years; the per capita dietary intake of peppers is about 40 g/day. Peppers are an important source of beta-carotene and vitamin A, which have antimutagenic and/or anticarcinogenic properties. In the present study, Salmonella typhimurium tester strain YG1024 in the plate-incorporation test was used to examine the antimutagenicity of carotenois extracted from five different types of Capsicum spp. ('Chilaca', 'Poblano', 'Serrano', 'Jalapeño' and 'Pimiento') which were chosen, based on their consumption and availability on the local market. Extracts from these peppers were tested against 1-6-dinitropyrene (1,6-DNP) and 1,8-dinitropyrene (1,8-DNP) mutagenicity. Dose-response mutagenicity curves of 1-NP; 1,6-DNP and 1,8-DNP were obtained. For the antimutagenicity studies, doses of 0.05 microgram/plate, 0.20 ng/plate and 0.06 ng/plate for 1-NP, 1,6-DPN and 1,8-DNP respectively were chosen, and the number of net revertants/plate were 1008 for 1-NP, 512 for 1,6-DNP, and 712 for 1,8-DPN. Trans-beta-carotene and the extracts were not toxic to the bacteria at the concentrations tested. The extracts obtained from the peppers showed more inhibition than pure trans-beta-carotene on 1-NP; 1,6-DNP and 1,8-DNP mutagenicity. Chilaca pepper extract required 0.36 g (34 nmol expressed as trans-beta-carotene equivalents) of fresh pepper to inhibit 94% on 1-NP mutagenicity, 78% on 1,6-DNP mutagenicity and 84% on 1,8-DNP mutagenicity. Bell pepper ('Pimiento') extract required 1.53 g (50 nmol expressed as trans-beta-carotene) to obtain 87%, 79% and 73% inhibition on 1-NP; 1,6-DNP and 1,8-DNP mutagenicity respectively. Since pure beta-carotene inhibited only approximately 50% the mutagenicity of nitroarenes, these results suggest that each one of the pepper extracts have more than one antimutagenic compound (e.g., beta-carotene and xanthophylls) and those functional nutrients apparently have a synergistic effect.

Antimutagenic activity of natural xanthophylls against aflatoxin B1 in Salmonella typhimurium.

Carotenoids (carotenes and xanthophylls) are excellent antioxidants with antimutagenic and anticarcinogenic properties. They occur naturally in some foods such as carrots, red tomatoes, butter, cheese, paprika, palm oil, corn kernels, Marigold petals, annatto, and red salmon. In the present study, we used the Salmonella plate incorporation test to examine the effect of xanthophylls extracted from Aztec Marigold (Tagetes erecta) on the AFB1 mutagenicity, using tester strain YG1024. The effect of lutein on the DNA-repair system in YG1024 was investigated by a pre-incubation test. In a dose-response curve of AFB1, the mutagenic potency was 1,031 revertants/nmol. The dose of 0.5 microgram AFB1/ plate was chosen for the antimutagenicity studies. Pure lutein and xanthophylls from Aztec Marigold flower (oleoresin and xanthophyll plus) inhibited the mutagenicity of AFB1 in a dose-dependent manner. The pigments were more efficient at inhibiting the AFB1 mutagenicity than pure lutein. The percentages of inhibition on AFB1 mutagenicity were 37, 66, and 76% for lutein, oleoresin, and xanthophyll plus at the dose of 2 micrograms/plate, respectively. Lutein had a modest effect on the DNA-repair system of YG1024. In spectrophotometric studies, a new absorption peak was detected at 378 nm when lutein and AFB1 were incubated together, and lutein reacted with AFB1 metabolites. The results suggest that the inhibitory mechanism of lutein against AFB1 mutagenicity is most probably the result of a combination of the following events: formation of a complex between lutein and AFB1, direct interaction between lutein and AFB1 metabolites, and finally that the lutein may also affect the metabolic activation of AFB1 by S9 and the expression of AFB1-modified Salmonella DNA.