S.E. Schriner et al., "Extension of murine lifespan by overexpression of catalase targeted to mitochondria." Science, 308:1909-11, 2005. (Cited in 107 papers)
Peter Rabinovitch at the University of Washington at Seattle and his colleagues found that transgenic mice overexpressing the antioxidant enzyme catalase in their mitochondria lived nearly 20% longer and exhibited less heart disease and other age-related declines. This supported the free-radical theory of aging.
Replicating the findings has proven difficult. Rabinovitch says that changes in veterinary care have led to euthanasia of mice that develop dermatitis and other ailments at early ages. This practice has confounded the replication of past longevity observations.
Richard Miller at the University of Michigan, Ann Arbor, offers his opinion: "If mito-Cat mutations do increase lifespan in mice, the effect may depend in complicated ways on a specific and not well-characterized set of background genes and environmental factors."
The work ahead:
Rabinovitch says he's about two-thirds of the way through aging studies with two different mouse strains. New data, he says, clarify the protection against age-related cardiac changes and nonhematologic cancers, and they are working on new transgenic models.
The 2005 data:
|Mice overexpressing||Mice (wt littermates)||% Increase lifespan (p value)|
|Peroxisomal catalase #1||8 (71)||10% (not significant)|
|Peroxisomal catalase #2||36 (22)||13% (0.02)|
|Peroxisomal catalase #3||54 (73)||11% (0.003)|
|Nuclear targeted catalase #1||36 (46)||4% (not significant)|
|Nuclear targeted catalase #2||42 (52)||3% (not significant)|
|Mito. targeted catalase #1||42 (58)||17% (0.0001)|
|Mito. targeted catalase #2||20 (44)||21% (0.0002)|