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Antioxidant Enzyme Prolong Animal Lifespan: Study

Posted on: Friday, 6 May 2005, 12:00 CDT

Antioxidant enzyme prolong animal lifespan: study

LOS ANGELES, May 5 (Xinhua)-- Higher levels of an antioxidant enzyme in cells have significantly extended the life of genetically modified mice in lab, US scientists reported on Thursday.

The mice also exhibited less heart disease and other age- related declines, said researchers at the University of Washington School of Medicine. Their study, published online by the journal Science on May 5, supports the controversial free-radical theory of aging.

The theory suggests that very reactive chemicals, called "free radicals," can be damaging to the body at the cellular level. Those reactive chemicals can take part in unnecessary chemical reactions that can damage the cell components including DNA.

Some researchers believe that free radicals could contribute to or hasten 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 people may be able to live longer.

In this new study, the researchers led by Peter Rabinovitch, a professor at the University of Washington School of Medicine, focused the study on catalase, an enzyme in the body that helps convert hydrogen peroxide into water and oxygen.

Hydrogen peroxide is a waste product of metabolism and it can be the precursor of free radicals that can damage the cell. The damage can in turn lead to more flaws in the cell's chemical processes, making a vicious cycle that leads to more free radicals and more cellular damage.

The researchers studied mice with a genetic variation that made them produce more human catalase, the enzyme that breaks down hydrogen peroxide. They targeted delivery of the catalase to different areas of the cell: the cytoplasm, where catalase normally goes to decompose hydrogen peroxide; the nucleus, the DNA- containing "control center" for the cell; and the mitochondrion, the cell's power plant that converts organic matter into energy.

They 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, dubbed the MCAT group, had about a 20 percent increase in average and maximum lifespan, or about four and a half months.

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 created as a byproduct of energy production. Removing hydrogen peroxide "at the source" seems to be the most effective strategy for enhancing lifespan.

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 in a statement, "it shows the significance of free radicals, and of reactive oxygen species in particular, in the aging process."

The study is very powerful in that it clearly demonstrates the important steps and pathways in the aging process. By identifying these steps and pathways, scientists can pave the way for future development of drugs or other treatments that protect the body from free radicals and possibly some age-related conditions, he noted.

Source: Xinhua News Agency - CEIS

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