In its normal molecular form, oxygen is harmless. However, cellular metabolism involving oxygen can generate several highly reactive forms of oxygen called free radicals. In an average human cell, several thousand lesions occur in the DNA every day. Many of these lesions result from oxidative damage. Unrepaired DNA can lose its ability to code for proteins.
Mutations also can result.
These mutations can activate oncogenes or silence tumor suppressor genes. In the case of children with Cockayne syndrome, Cooper says these latest findings establish that oxidative damage to active genes is not preferentially repaired, and in the most severe cases, repair is slowed throughout the whole genome. We have not yet proved this is the case. We believe that the inability to repair oxidative damage is the underyling cause of Cockayne's. Cooper, who is a member of Berkeley Lab's Life Sciences Division, says one novel implication of the research is that two repair mechanisms thought to be independent of one another appear to work together to repair oxidative DNA damage.