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Posted on Feb 21, 2005, 6 a.m.
By Bill Freeman
Findings suggest that curbing free radical production could increase human longevity. A genetic manipulation that reduces free radical damage to nerve cells extends the lifespan of flies, suggesting a new approach to increasing longevity in humans. The manipulation reduces damage by free radicals that are a byproduct of energy production by mitochondria.
Findings suggest that curbing free radical production could increase human longevity.
A genetic manipulation that reduces free radical damage to nerve cells extends the lifespan of flies, suggesting a new approach to increasing longevity in humans.
The manipulation reduces damage by free radicals that are a byproduct of energy production by mitochondria.
It focuses on proteins called mitochondrial uncoupling proteins (UCPs) that are involved in regulating free radical production.
To examine the effect of mitochondrial uncoupling on free radical production and aging, Stephen Helfand of the University of Connecticut Health Center in Farmington and colleagues inserted a human gene called UCP2 into flies in a way that it could be turned on in nerve cell mitochondria in adulthood.
A genetic manipulation that reduces free radical damage to nerve cells extends the lifespan of flies, suggesting a new approach to increasing longevity in humans.
The manipulation reduces damage by free radicals that are a byproduct of energy production by mitochondria.
It focuses on proteins called mitochondrial uncoupling proteins (UCPs) that are involved in regulating free radical production.
To examine the effect of mitochondrial uncoupling on free radical production and aging, Stephen Helfand of the University of Connecticut Health Center in Farmington and colleagues inserted a human gene called UCP2 into flies in a way that it could be turned on in nerve cell mitochondria in adulthood.
