Article

Dietary agents in cancer prevention: flavonoids and isoflavonoids.

Department of Food Science and Human Nutrition, 2312 Food Sciences Building, Iowa State University, Ames, IA 50011, USA.
Pharmacology [?] Therapeutics (Impact Factor: 7.79). 90(2-3):157-77. DOI: 10.1016/S0163-7258(01)00137-1
Source: PubMed

ABSTRACT Flavones and isoflavones may play a prominent role in cancer prevention since these compounds are found in numerous plants that are associated with reduced cancer rates. This article reviews recent epidemiological and animal data on isoflavones and flavones and their role in cancer prevention. It covers aspects of the bioavailability of these dietary constituents and explores their mechanism of action. Human epidemiology data comes primarily from studies in which foods rich in isoflavones or flavones are associated with cancer rates. This approach has been particularly useful with isoflavones because of their abundance in specific foods, including soy foods. The bioavailability of flavones and isoflavones has been shown to be influenced by their chemical form in foods (generally glycoside conjugates), their hydrophobicity, susceptibility to degradation, the microbial flora of the consumer, and the food matrix. Some information is available on how these factors influence isoflavone bioavailability, but the information on flavones is more limited. Many mechanisms of action have been identified for isoflavone/flavone prevention of cancer, including estrogenic/antiestrogenic activity, antiproliferation, induction of cell-cycle arrest and apoptosis, prevention of oxidation, induction of detoxification enzymes, regulation of the host immune system, and changes in cellular signaling. It is expected that some combination of these mechanisms will be found to be responsible for cancer prevention by these compounds. Compelling data suggest that flavones and isoflavones contribute to cancer prevention; however, further investigations will be required to clarify the nature of the impact and interactions between these bioactive constituents and other dietary components.

1 Bookmark
 · 
213 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The contribution of calories from nutrient-poor snack foods is rising in many Western diets, possibly contributing to the increasing prevalence of obesity and diabetes. Soy offers unique potential to provide high quality protein, dietary fiber, and phytochemicals to snack foods to produce a more healthful nutritional profile. In this study, 27.3% of wheat flour was replaced with soy ingredients in a soft pretzel in order to observe the changes in the product"s satiety, glycemic index (GI), and insulinemic index (II). First, the soy pretzel was tested for consumer acceptability by 51 untrained sensory panelists on a 9-point hedonic scale. Second, in a crossover trial, 20 healthy adults consumed soy and traditional pretzels (1000 kJ or 239 kcal each) after an overnight fast. They reported their levels of satiety on a 10 cm visual analogy scale (VAS) for 2 hrs postprandially. Third, 12 healthy, non-diabetic subjects consumed soy or traditional pretzels (50 ± 2 g available carbohydrates) to determine the GI and II of both products. Blood glucose and insulin responses were monitored for 2 hrs after consumption and compared to a glucose reference. It was found that the consumer-acceptable soy soft pretzel has a lower GI than its 2 traditional counterpart [39.1±20.4 (mean±SD) for soy and 66.4±15.3 for wheat, p=0.002]. On the other hand, soy addition did not statistically affect II (p=0.15), or satiety (p=0.91). In conclusion, a soy pretzel formulation with 27.3% of wheat flour replaced by soy ingredients leads to attenuated postprandial glycemia without significantly affecting insulinemia or satiety in healthy adults.
  • [Show abstract] [Hide abstract]
    ABSTRACT: a b s t r a c t New strategies for the prevention of colon cancer persists a crucial need. However, resistance to current chemopreventive drugs is relatively prevalent in colon carcinogenesis. For this intent, a chemopreventive study was acquitted to elucidate the probable effect of taxifolin (TAX) against 1,2-dimethylhydrazine (DMH) induced colon carcinogenesis in mice and to evaluate its efficacy with 5-fluorouracil (5-FU) drug control. Swiss Albino mice were intended for colon carcinogenesis received subcutaneous injections of DMH (20 mg/kg bw., sc) once a week for 15 weeks and were treated with TAX (4 ␮g/kg bw, op) and 5-FU drug control (10 mg/kg bw., op) for the entire study period. Our results unveil that mice administered with TAX significantly modulates DMH induced histological alterations (ACF, AgNORs, and mucin depletion). Moreover, TAX treatment also inhibits DMH mediated oxidative damage by diminishing tissue lipid peroxidation (MDA, MPO and CD) accompanied by enhanced activities of enhanced activities of free radical metabolizing enzymes (SOD, CAT, GPx, GR, GSH, vitamin A, C and E). Apoptotic and proliferating cell nuclear antigen (PCNA) findings also revealed that treatment with TAX substantially regulates cell proliferation through the increased extent of DNA fragmentation. The incidence of colon cancer in TAX treated mice was significantly reduced when compared to that of 5-FU control. Our findings concluded that taxifolin act as an effective chemopreventive agent against colon carcinogenesis by its virtue of antioxidant mediated apoptosis and anti-proliferative activities.
    Biomedicine and Preventive Nutrition. 12/2014; 4:499-509.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: A natural predominant flavanone naringenin, especially abundant in citrus fruits, has a wide range of pharmacological activities. The search for antiproliferative agents that reduce skin carcinoma is a task of great importance. The objective of this study was to analyze the anti-proliferative and apoptotic mechanism of naringenin using MTT assay, DNA fragmentation, nuclear condensation, change in mitochondrial membrane potential, cell cycle kinetics and caspase-3 as biomarkers and to investigate the ability to induce reactive oxygen species (ROS) initiating apoptotic cascade in human epidermoid carcinoma A431 cells. Results showed that naringenin exposure significantly reduced the cell viability of A431 cells (p<0.01) with a concomitant increase in nuclear condensation and DNA fragmentation in a dose dependent manner. The intracellular ROS generation assay showed statistically significant (p<0.001) dose-related increment in ROS production for naringenin. It also caused naringenin-mediated epidermoid carcinoma apoptosis by inducing mitochondrial depolarization. Cell cycle study showed that naringenin induced cell cycle arrest in G0/G1 phase of cell cycle and caspase-3 analysis revealed a dose dependent increment in caspase-3 activity which led to cell apoptosis. This study confirms the efficacy of naringenin that lead to cell death in epidermoid carcinoma cells via inducing ROS generation, mitochondrial depolarization, nuclear condensation, DNA fragmentation, cell cycle arrest in G0/G1 phase and caspase-3 activation.
    PLoS ONE 10/2014; · 3.53 Impact Factor

Full-text (2 Sources)

Download
688 Downloads
Available from
May 28, 2014