Calorie restriction is the only reliable way across a wide range of species to increase life expectancy. So the mechanism by which a low calorie diet extends life is a question which many researchers are pursuing. Since very few of us are willing to live in a state of perpetual hunger we need a drug that would give us the benefit of calorie restriction without the gaunt look and hunger pangs. So a report from a German group on an enzyme in a yeast model that appears to be key to life extension for calorie-restricted yeast merits some attention. The researchers are able to show that turning up the enzyme Srx1 protects an enyzme called Prx1 and the Prx1 is key to preventing aging damage. The result is more Prx1 activity, less damage, and longer life - at least in yeast.
By consuming fewer calories, ageing can be slowed down and the development of age-related diseases such as cancer and type 2 diabetes can be delayed. The earlier calorie intake is reduced, the greater the effect. Researchers at the University of Gothenburg have now identified one of the enzymes that hold the key to the ageing process.
"We are able to show that caloric restriction slows down ageing by preventing an enzyme, peroxiredoxin, from being inactivated. This enzyme is also extremely important in counteracting damage to our genetic material," says Mikael Molin of the Department of Cell and Molecular Biology.
This makes sense from a theoretical perspective. Turning up repair enzymes will reduce the rate at which permanent debilitating (and eventually fatal) damage accumulates. Whether more activity of these particular enzymes would extend life in humans remains to be seen. But it seems very likely that if not these enzymes then some other repair enzymes could extend our lives if we could find safe ways to turn them up to higher levels in our cells.
Prx1 breaks down hydrogen peroxide, a toxic by-product of normal human metabolism.
They are able to show that active peroxiredoxin 1, Prx1, an enzyme that breaks down harmful hydrogen peroxide in the cells, is required for caloric restriction to work effectively.
More Srx1 by itself extends yeast cell life without calorie restriction.
The results, which have been published in the scientific journal Molecular Cell, show that Prx1 is damaged during ageing and loses its activity. Caloric restriction counteracts this by increasing the production of another enzyme, Srx1, which repairs Prx1. Interestingly, the study also shows that ageing can be delayed without caloric restriction by only increasing the quantity of Srx1 in the cell. Repair of the peroxiredoxin Prx1 consequently emerges as a key process in ageing.
A drug that mimics the effects of calorie restriction will only slow down the rate of aging and probably not by a large amount. But slowed aging could give some of us enough time to live until rejuvenation therapies become available.
|Share |||Randall Parker, 2011 November 08 07:16 PM Aging Mechanisms|