From: J. R. Molloy (jr@shasta.com)
Date: Thu Nov 18 1999 - 09:21:20 MST
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Researchers Extend Lifespan of Mice
By WILLIAM McCALL
Associated Press Writer
Italian scientists have genetically engineered mice to live up
to 35 percent longer than normal _ an experiment that offers the
strongest evidence yet that aging in mammals is controlled by a
genetic switch.
The researchers at the European Institute of Oncology in Milan
deleted a gene in the mice that makes them vulnerable to cell
damage caused by oxygen.
Equally important, the mice suffered no apparent side effects.
Other scientists called the study a major step forward in
understanding the aging process. The study was published in
Thursday's issue of the journal Nature.
``They hit a milestone in aging research with this study _
they've found a genetic intervention in mice that make them live
longer without any side effects,'' said Leonard Guarente of the
Massachusetts Institute of Technology.
Genetic control of longevity had already been confirmed in worms
and flies, but not in mammals, which have their own aging process.
``We now know for sure that longevity is genetically
controlled,'' said the study's author, Pier Giuseppe Pelicci.
Researchers breeded the mice without a gene that produces protein
vulnerable to cell damage from oxidation.
The findings could mark a departure from one of the basic rules
of biology _ namely, that if you tinker with a gene or other factor
in an animal to add some kind of benefit, it usually comes at a
cost somewhere else.
For example, scientists can increase mouse longevity by about 30
percent by tightly restricting diet and slowing down the
metabolism, but it comes at a cost of decreased fertility and size.
The Italian researchers could find no other problems with the
mutant mice, though Pelicci admitted that the gene's entire
function is unknown, so problems could still arise.
The researchers are now investigating the possibility of
blocking the age-controlling protein chemically, which could lead
to the development of life-extending drugs.
But Pelicci warned: ``How many times have we found something in
mice that was not the case in humans?''
Oxidation has been suspected in aging since 1956, when it was
first proposed that free radicals _ unstable molecules with an
unpaired electron _ attack cells. Oxidative damage has been
implicated in forms of cancer and in heart disease.
Joe McCord of the Webb-Waring Institute for Biomedical Research
at the University of Colorado, who in 1969 helped prove that
oxidation was involved in cell damage, called the Italian study
``fascinating and very significant,'' but noted that oxidation also
regulates beneficial cellular functions as well as destructive
ones.
``The balance that works best in the laboratory may not be the
best balance if the animal is dealing with wound healing and
infections and other kinds of stress,'' he said.
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