Molecular medicine-Normal Aging in spite of Certain Defects in DNA Repair or Increases in Antioxidant Enzyme Production

If a DNA repair pathway lacks an enzyme,
but the missing enzyme is partially
compensated for by a similar enzyme,
then repair may be sufficient to allow
survival, growth, and normal aging. While
such fairly good compensation may allow
normal aging, the repair of DNA damages
would still be less than if the repair
pathway were intact, and that could lead to
Aging and Sex, DNA Repair in 65
increased carcinogenesis. Such fairly good
compensation for DNA repair enzyme
defects may be the basis for normal aging,
but increased carcinogenesis, shown by
mice with the DNA repair mutations listed
in Table 4. As shown in Fig. 1, XPA and
XPC proteins each occur as one member
of a pair of complexed proteins whose
function is recognition of DNA damage
to be repaired by an NER pathway. It is
possible that the other complexes that can
recognize DNA damage can compensate,
at some level, when one of the recognition
complexes is absent.
Further, in some instances, genetic
alterations caused increased SOD production
in fruit flies but did not affect aging.
However, the inserted SOD gene may have
been turned on under the control of promoters
expressing in tissues where it may
not have been useful, or at rather low levels.