Abstract
We have previously reported that supplementation with folic acid (1.2 mg day(-1) for 12 week) elicited a significant improvement in the folate status of 61 healthy volunteers. We have examined effects of this supplement on markers of genomic stability. Little is known about the effect of folate supplementation on DNA stability in a cohort, which is not folate deficient. Preintervention, there was a significant inverse association between uracil misincorporation in lymphocyte DNA and red cell folate (P < 0.05). In contrast, there were no associations between folate status and DNA strand breakage, global DNA methylation or DNA base excision repair (measured as the capacity of the lymphocyte extract to repair 8-oxoGua ex vivo). Folate supplementation elicited a significant reduction in uracil misincorporation ( P < 0.05), while DNA strand breakage and global DNA methylation remained unchanged. Increasing folate status significantly decreased the base excision repair capacity in those volunteers with the lowest preintervention folate status (P < 0.05). Uracil misincorporation was more sensitive to changes in folate status than other measures of DNA stability and therefore could be considered a specific and functional marker of folate status, which may also be relevant to cancer risk in healthy people.
Original language | English |
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Pages (from-to) | 1942-1947 |
Number of pages | 6 |
Journal | British Journal of Cancer |
Volume | 94 |
Issue number | 12 |
Early online date | 30 May 2006 |
DOIs | |
Publication status | Published - 19 Jun 2006 |
Keywords
- folic acid
- health
- uracil misincorporation
- DNA damage
- HAMSTER OVARY CELLS
- FOLIC-ACID SUPPLEMENTATION
- DONOR-DEFICIENT RATS
- URACIL MISINCORPORATION
- METHYLENETETRAHYDROFOLATE REDUCTASE
- IN-VITRO
- S-ADENOSYLMETHIONINE
- CONTROLLED-TRIAL
- COMMON MUTATION
- COMET ASSAY