Mice engineered to produce high levels of the antioxidant catalase live significantly longer than their wildtype counterparts, according to a report published online by Science this week. Researchers observed the largest lifespan extension when they targeted the catalase to mitochondria, which are thought to be the major cellular source of reactive oxygen species (ROS) such as hydrogen peroxide.

The results lend support to the free-radical theory of aging, which attributes many of the infirmities of old age to accumulated cellular damage caused by ROS and the free radicals they generate. Although such damage increases with age, previous attempts to manipulate it have yielded contradictory results. "Until this study, it wasn't clear that it was truly a cause [of aging in mammals] or an effect that correlated with age," David Sinclair of Harvard Medical School, Boston, who was not involved in the study, told The Scientist. "It's a pretty big...

Interested in reading more?

Become a Member of

Receive full access to more than 35 years of archives, as well as TS Digest, digital editions of The Scientist, feature stories, and much more!
Already a member?