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Flavonoids Exhibit Strong Chemopreventive Effects

Flavonoids and foods

Flavonoids have significant chemopreventive effects in vivo, inhibiting the development of malignant tumors without noticeable toxicity and side effects. Research shows that flavonoids can prevent histopathological changes induced by DMH and suppress the occurrence of colon cancer in rats by regulating antioxidant functions and lipid peroxidation. They also inhibit chromosome aberrations caused by pickled fish, pickled lamb, fried fish, and lamb kebabs in rats, with a protective effect superior to that of quercetin.

The chemopreventive effects of flavonoids are mainly related to the following mechanisms:

  1. Antioxidant Action: Flavonoids exhibit strong antioxidant properties, inhibiting lipid peroxidation and removing oxygen free radicals. Oxidative stress leads to oxidative damage to macromolecules such as DNA and lipids, which are fundamental to cancer development. Flavonoids help prevent cancer by mitigating these oxidative processes.
  2. Anti-Radiation Effects: Flavonoids can eliminate free radicals produced by radiation, reducing DNA damage and the side effects of radiotherapy. They also inhibit the formation of 8-OHDG caused by ultraviolet radiation and Fenton reactions. This dual action reduces radiation-induced DNA damage and inhibits cancer cell proliferation, thus improving the efficacy of chemotherapy and radiotherapy.
  3. Reduction of Chemotherapy Toxicity: Oral intake of flavonoids has been shown to reduce the toxicity of adriamycin and lessen the side effects of various chemotherapy drugs.

Overall, flavonoids enhance the efficacy of chemotherapy and radiotherapy through multiple mechanisms and play a crucial role in chemoprevention.

Additionally, in human and mouse leukemia cells and human urinary cancer cells, flavonoids may act as non-competitive inhibitors of arylamine N-acetyltransferase (NAT). This inhibition alters the enzyme’s kinetic parameters K and V and exhibits dose-dependent inhibition activity, preventing cancer cells from normal acetylation of arylamine substrates.

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