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Catalase enzyme prolongs mouse lifespan


A research, led by scientists from University of Washington in Seattle, has found that mice genetically engineered to produce high levels of a human antioxidant enzyme lived longer than normal mice. This study supports the free-radical theory of aging.

The theory suggests that free radicals, very active compounds, can take part in chemical reactions that can damage the cell components, including DNA.
Some researchers believe that free radicals could contribute to heart disease, cancer, and other age-related diseases.
The theory also suggests that if the body could be protected from those free radicals, then age-related diseases could be tamed and organisms - and ultimately people - may be able to live longer.

Peter Rabinovitch, at the University of Washington - School of Medicine, and his colleagues focused their study on catalase, an enzyme in the body that helps convert hydrogen peroxide into water and oxygen.
Hydrogen peroxide is a product of catabolism and it can be a precursor of free radicals that can damage the cell.

The researchers studied mice with a genetic variation that made them produce more human catalase and compared the different groups of mice to a control group and found that increased production of catalase could affect the mouse lifespan.

The mice with higher catalase levels in the mitochondria ( MCAT group ), had about a 20 percent increase in lifespan.
The mice with increased catalase levels in the nucleus and cytoplasm saw only modest increases in lifespan.

These results fit with the theory that mitochondria can be an important source of free radicals.
Removing hydrogen peroxide " at the source " seems to be the most effective strategy for enhancing lifespan, Rabinovitch said.

The scientists also found that the mitochondrion-targeted catalase mice had healthier heart muscle tissue, indicating that the catalase helped protect from age-related heart problems seen in wild-type mice. The MCAT mitochondria also had fewer mutations, and the MCAT nuclear DNA had fewer oxidized components.

" This study is very supportive of the free-radical theory of aging, " said Rabinovitch. " It shows the significance of free radicals, and of reactive oxygen species in particular, in the aging process. "

The study was funded by the National Institute on Aging. In addition to other researchers from the UW School of Medicine, the project also included researchers from the University of California, Irvine, and the University of Texas Health Sciences Center at San Antonio.

Source: Science, 2005


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