Aging Evidence is rapidly mounting that DNA instability, the susceptibility of DNA to damage combined with the limits of DNA repair processes, is a major factor in the development of cancer and probably of aging. New evidence indicates that certain locations on chromosomes, known as fragile sites, are particularly likely to break apart or suffer mutations. For example, a long string of DNA on human chromosome 3 called FRA3B is often disrupted in breast cancer. Scientists are intensively studying these fragile sites to find out why they are so easily damaged and how they are normally repaired. Folic acid is emerging as an important protectant of fragile DNA sites.
Folic acid is essential for DNA synthesis and repair.
This may be a major reason for the increased risk of children to certain cancers, such as medulloblastoma, when their mother has a low intake of folate during pregnancy. Folate is required for the proper incorporation into DNA of the pyrimidine base uracil. Faulty uracil incorporation and then attempts to repair the DNA by removing the incorrectly placed uracil, taking place under conditions of deficient folate, may ultimately result in DNA double strand breakage, chromosome instability, and cancer. One way that folate is known to regulate DNA synthesis and repair is via folate's essential role in the production of S- adenosylmethionine, the primary methyl donor for DNA methylation. Human studies have shown that folic acid can reduce the risk of developing certain premalignant changes in tissues, such as cervical and bronchial dysplasia found in oral contraceptive users and smokers, respectively.