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Heart of the Matter. Mitochondria in the transgenic heart (right) carries catalase (green). Normal heart muscle is shown on the left.

Living to Eat Cheese Another Day

In a boost for a controversial theory of aging, mice engineered to make a human protein that sponges up cell-damaging molecules live 19% longer than other mice. The new research, published online today in Science, is consistent with the idea that these so-called free radicals are a cause of aging, but additional work is needed to clarify how the protein actually extends lives.

Some scientists think that aging is caused by a nasty byproduct of metabolism that beats up the components of cells, much like combustion wears down engines. These byproducts are known as free radicals or oxidants, and they are made mostly in the mitochondria, which turn food into energy. Previous work has shown that providing worms or flies with an overabundance of proteins that mop up free radicals or oxidants extends the animals' lives, though not always. Five years ago, a group found that overproducing the anti-oxidant protein SOD in mice didn't help rodents live longer. Molecular biologist Samuel Schriner at the University of California, Irvine, and colleagues wanted to know if a different anti-oxidant mop called catalase, which cleans up hydrogen peroxide (a source of free radicals), would do the trick.

To find out, the researchers genetically engineered mice to overproduce the human form of catalase. Mice that made extra catalase in their mitochondria lived longer than normal mice, by about 19%. The researchers examined various tissues and found the mitochondrial catalase had upwards of 50 times the activity in the heart and skeletal muscles, resulting in heart tissue with about 25% less hydrogen peroxide in almost-3 year old mice, compared to normal mice. So the team took a closer look at the heart and found that 2-year old rodents with human catalase sported hearts that were nearly twice as healthy as those without. But why the animals live longer is still open to interpretation, say the authors. "It's possible they live longer not because we modulated aging itself, but because we beefed up their hearts," says Schriner.

"This is the first transgenic [mammal] that lives longer," says physiologist Arlan Richardson of the University of Texas Health Science Center, San Antonio, adding that the result is one of the strongest life extensions in mice.

Related sites
A review of oxidative stress, at Science of Aging Knowledge Environment (Subscription)
Oxidative stress and DNA mutations, at Science of Aging Knowledge Environment (Subscription)