WASHINGTON (Cox News Service) -- Gray hair, brittle bones, infertility and ultimately death apparently result from the fact that our genes are constantly being injured and cannot repair themselves fast enough, Dutch scientists say.

The scientists reported Friday(cq) that by disrupting the way genes keep themselves in shape inside the cells of laboratory mice, they caused a process that seemed to mimic the way humans age.

Coincidentally, Emory University biochemist Paul Doetsch this week received a U.S. patent on a group of enzymes that someday may be used to help genes repair themselves.

So far, nobody's talking seriously about a biochemical fountain of youth. But as biochemists fit together the molecular pieces of the aging puzzle, they see vague images of a time when it may be possible to forestall the cellular wear and tear that eventually causes every creature to die.

Damage to DNA, the material genes are made of, has been a suspected cause of aging since the early 1990s. But the precise mechanism has not been clear.

Now biochemists at Erasmus University in Rotterdam, Holland, think they have the answer.

Their experiment with laboratory mice suggests that aging is a consequence of the gradual breakdown of an imperfect system for repairing DNA.

Environmental forces such as ultraviolet light and harmful waste products generated by each cell's internal processes are constantly assaulting our genes, said Jan H.J. Hoeijmakers, one of biochemists.

Some of the chief culprits appear to be substances called free radicals, which are created inside the cells themselves. These are the unseen and unfelt chemicals that Americans battle by spending millions of dollars each year on Vitamins C and E and other "antioxidants."

The free radical compounds tear into DNA and injure it, Hoeijmakers said.

"This damage is occurring at every moment in every cell in our bodies," he said in a telephone interview.

When a gene is damaged, it's like destroying part of a blueprint. The damaged gene no longer contains a workable set of instructions for the production of a protein that the cell needs in order to function and keep itself repaired.

These special repair proteins have evolved over eons to address the damage to the genes. Some move along the ribbon-like DNA molecule, searching for damaged places. When they find one, other proteins are recruited to come in and patch things up, Hoeijmakers said. Some snip out the damaged segment, and others rebuild it according to the original plan.

But the process is imperfect. The repair proteins cannot keep up with the constant onslaught, and as years pass the damage builds up, gene by gene, cell by cell. The critical proteins become scarce. The machine starts to wear out.

The process really picks up speed, Hoeijmakers said, when DNA segments containing blueprints for the genes' own repair proteins are damaged.

In an article in Friday's edition of Science, Hoeijmakers and his colleagues describe an experiment in which they deliberately caused mutations among mice in a gene that plays a key role in the repair process.

They were trying to duplicate a rare human genetic disorder that causes its victims to become frail and die at relatively young age.

"The first thing we noticed was that these mice became gray at much higher numbers and much earlier than their control litter mates," he said. "That was the start for us to say, 'Oh, maybe there is aging going on in these mice.' "

Further study revealed all the symptoms of aging, and most of the genetically altered mice appeared to die of old age when they had lived only about one-third as long as normal mice, he said.

Doetsch and scientists working in his lab at Emory in Atlanta were granted a U.S. patent Tuesday for a collection of compounds that the Patent Office said may eventually be useful at various points in the DNA repair process.

Some of the substances identified in the Doetsch patent have been shown to play a role in detecting some kinds of DNA damage, while others perform various tasks involved in snipping away damaged segments or constructing new DNA, according to the patent, which was assigned to Emory.

The research involved in identifying and reproducing the repair tools was supported by grants to the university by the National Cancer Institute.

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