~ More Evidence for Free Radical Theory of Aging

A study published online on May 5 2005 in the journal Science (http://www.sciencemag.org/) reports the finding of researchers at the University of Washington and other centers of a way to significantly extend the lifespan of laboratory animals while reducing the effects of aging.

University of Washington School of Medicine professor of pathology Dr. Peter Rabinovitch and colleagues studied mice bred to produce human catalase, the enzyme that converts hydrogen peroxide into water and oxygen. Hydrogen peroxide is produced during metabolism and is a precursor of free radicals that lead to cell damage, which causes the generation of even more free radicals. The team targeted delivery of the catalase to the cytoplasm of the cell where catalase normally decomposes hydrogen peroxide, the nucleus, which is the center of the cell, and the mitochondrion, which are the cell's energy producing organelles.

While mice with elevated catalase levels in the nucleus and cytoplasm experienced small increases in lifespan, animals that produced catalase in their mitochondria were found to experience a 20 percent increase in average and maximum lifespan and had healthier heart tissue. This adds credence to the theory that the mitochondria are a major source of free radicals generated as a byproduct of energy production. Dr Rabinovitch stated, "This study is very supportive of the free-radical theory of aging. It shows the significance of free-radicals, and of reactive oxygen species in particular, in the aging process."

He added, "People used to only focus on specific age-related diseases, because it was believed that the aging process itself could not be affected. What we're realizing now is that by intervening in the underlying aging process, we may be able to produce very significant increases in 'healthspan,' or healthy lifespan."

The discovery may lead to the development of new antioxidant drugs that could protect the body from free radicals and reduce some age-related conditions.

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