Age-related increases in DNA repair and antioxidant protection: a comparison of the Boyd Orr Cohort of elderly subjects with a younger population sample.

Abstract

One commonly held theory of ageing is that it is caused by oxidative damage to critical molecules in the body, including proteins, lipids and nucleic acids. Accumulation of oxidative DNA damage with age will occur if there is an increase in reactive oxygen species in the body, or a decline in antioxidant defences, or a reduced efficiency of DNA repair.
Using the comet assay, we have measured DNA breaks and oxidised purines in lymphocytes from subjects of different age groups: 20-35 (n = 40), 63-70 (n = 35), and 75-82 (n = 22). We also measured the resistance of lymphocyte DNA to H(2)O(2)-induced oxidative damage, and the repair activity of cell-free lymphocyte extracts on a substrate containing 8-oxoguanine.
We found an increase in oxidative base damage in old age, but this apparently does not result from deterioration of either antioxidant defence or DNA repair. In fact, both of these tend to increase with age. There were few age-related differences in plasma levels of dietary antioxidants: tocopherols and retinol were higher in the older subjects, while lycopene was highest in the youngest age group.
It is possible, that in old age, antioxidant defences and DNA repair are induced, in response to a higher level of oxidative damage, as mitochondria become more leaky and release more reactive oxygen. It is equally possible that older people, as survivors, had relatively high levels of antioxidant defences and DNA repair earlier in their lives, compared with those who did not survive to such an age.