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Prenatal exposure to flavonoids: implication for cancer risk
Kimberly Vanhees1, Laura de Bock, Roger W L Godschalk
1Department of Health Risk Analysis and Toxicology, Nutrition and Toxicology Research, Institute Maastricht, Maastricht University, 6200 MD Maastricht, The Netherlands. kimberly.vanhees@maastrichtuniversity.nl
Summary
Dietary flavonoids like genistein and quercetin can cause DNA damage. This risk is amplified in individuals with compromised DNA repair, potentially increasing leukemia-related gene rearrangements.
Area of Science:
- Molecular Biology
- Genetics
- Toxicology
Background:
- Flavonoids are potent antioxidants found in dietary supplements.
- Flavonoids can induce DNA double-strand breaks (DSB) and rearrangements in the mixed-lineage leukemia (MLL) gene.
- Childhood leukemia is frequently associated with MLL gene rearrangements.
Purpose of the Study:
- To investigate if deficient DNA repair, due to Atm mutation, exacerbates the clastogenic effects of dietary flavonoids.
- To determine the impact of prenatal flavonoid exposure on Mll rearrangements in mice with compromised DNA repair.
Main Methods:
- In vitro and transplacental exposure of mice with different genetic capacities for DSB repair (Atm-ΔSRI vs. wild type) to genistein and quercetin.
- Assessed Mll rearrangements in bone marrow cells.
- Examined the incidence of malignancies following prenatal exposure.
Main Results:
- In vitro exposure to genistein/quercetin induced more Mll rearrangements in Atm-ΔSRI mutant mice than in wild-type mice.
- Prenatal exposure to genistein or quercetin in heterozygous Atm-ΔSRI mice led to higher frequencies of Mll rearrangements.
- A slight increase in malignancies was observed in DNA repair-deficient mice after prenatal flavonoid exposure.
Conclusions:
- Prenatal exposure to genistein and quercetin supplements may elevate the risk of Mll rearrangements.
- This risk is particularly pronounced in individuals with compromised DNA repair mechanisms.
- Dietary flavonoids warrant careful consideration, especially during pregnancy and in individuals with genetic predispositions to DNA repair deficiencies.
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