58
Aging and Sex, DNA Repair in
Tab. 2
Life span extension: increased life span from alterations in genes controlling DNA repair, apoptosis, or oxidant status.
Organism
Genetic
Pathway
Aging
Fertility
Spontaneous
Effect on
alteration
phenotype
phenotype
cancer
phenotype
Cellular
Induced
Spont.
Induced
ROS
DNA
mutation
apoptosis
damage
Mouse
100-fold excess
copies MGMT
gene
O
6
-meG DNA
repair
Life span
extension
n.t.
Reduced
n.t.
Reduced
O
6
-meG
No effect at
H-ras
locus
n.t.
Fruit fly
Excess SOD in
neurons or all
tissues or with
catalase in all
tissues
Removes ROS
Life span
extension
No change
n.t.
Reduced
occurrence of
oxidized
proteins
n.t.
n.t.
n.t.
Fruit fly
MsrA excess
Methionine
sulfoxide
reductase
Life span
extension
Extended
n.t.
Repaired protein
oxidation
n.t.
n.t.
n.t.
Mouse
p66
shc
defect
Blocks oxidant
and apoptosis
parts of p53
pathways
Life span
extension
n.t.
n.t.
Reduced
Reduced
oxidative
damage
n.t.
Reduced
Human
Higher speci±c
activity of PARP
BER
Life span
extension
n.t.
n.t.
n.t.
n.t.
n.t.
n.t.
Notes
: ROS: reactive oxygen species; Spont.: spontaneous; MGMT: O
6
-methylguanine-DNA methyltransferase; n.t.: not tested; SOD: superoxide
dismutase.
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