New Research Shows Targeted Antioxidants Help Mice Live Longer, Healthier Lives

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The frailty that often comes with old age may one day be delayed by targeting antioxidants to the mitochondria. (Wikimedia Commons)
Mice can avoid the frailty that comes with old age when antioxidants are targeted to their mitochondria. One day perhaps a similar treatment can help people have a healthier old age. (Wikimedia Commons)

You can’t go to a health website without reading about the praises of antioxidants. These miracle chemicals found in foods such as various berries, beans and artichokes are touted to help you lose weight, give you younger-looking skin, help fight off infections and so much more.

While many of the benefits of antioxidants are undoubtedly oversold, we do know that if given at high enough levels and targeted to the right place, antioxidants can help a mouse live 10-20% longer. If this holds up in people, that is equivalent to an extra 7-14 years for people here in the U.S.

And that isn’t all. These mice not only live longer but as Umanskya and coworkers show in a new study in the journal Proceedings of the National Academy of Sciences (PNAS), they also stay stronger and healthier for longer too. So the antioxidant treatment isn’t just adding extra time at the end of the mouse’s life. It is adding better, more productive years.

Protecting the mitochondria of mice  with antioxidants helps the mice live longer, healthier lives. (Flickr)
Protecting the mitochondria of mice with antioxidants helps the mice live longer, healthier lives. (Flickr)

Now don’t think that you can get the same effects from eating truckloads of blueberries (although they are both tasty and good for you). You can’t. These mice were genetically engineered to make antioxidants in the key part of the cell that needs protection—the mitochondria. They lived longer not because of what they ate but because of genetic modification.

This means that we need to wait until scientists figure out how to package antioxidants and deliver them specifically to the mitochondria to cash in on these benefits. And luckily for us, scientists are working furiously on this right now. Not only would this sort of targeting help with aging, but it would help treat many other devastating mitochondrial diseases as well.


And who knows? Maybe in the not too distant future, scientists will be able to genetically engineer the mitochondria in human eggs so that the resulting child lives a longer, healthier life.

Right now, scientists are able to replace diseased mitochondria with healthy ones in the eggs of women suffering from mitochondrial disease (although they are being prevented from doing this right now for ethical reasons).  So it may not be too long before they can do the same with genetically engineered mitochondria. It won’t be happening tomorrow but the technology could be closer than you think.

Making Energy Produces Pollution

Targeting the mitochondria makes sense because these poor things take a beating during our lifetime. Mitochondria are the energy plants of the cells. After our food gets digested, the remains are sent to mitochondria to be turned into ATP, the main source of cellular energy.

Just like burning fossil fuels for energy creates all sorts of pollutants, making energy in the mitochondria does too.  But instead of carbon dioxide, particulates and acid rain, the byproducts of making energy in the mitochondria are free radicals. And these are very, very nasty little chemicals.

The pollution from making energy in mitochondria are free radicals. (Wikimedia Commons)
The pollution from making energy in mitochondria are free radicals. (Wikimedia Commons)

Free radicals tend to quickly react with and so damage whatever is close by and in cells, that means the mitochondria and their DNA. These wounded mitochondria can no longer do their jobs properly and this is thought to be one of the big reasons we age.

Given this, it made perfect sense for the scientists to try to have mice live longer by adding something to the mitochondria that can defuse those free radicals. In this case, they added the catalase gene whose product is responsible for turning hydrogen peroxide (a precursor to free radicals) into water and oxygen.

Mice that had catalase added to their mitochondria lived longer. They also had fewer problems with age-related insulin resistance and energy imbalance. Overall, these mice did much better than their untreated littermates as they aged.

In the current study, Umanskya and coworkers found that the genetically engineered mice also suffered less age-related muscle weakness than regular old mice. This is more evidence that dealing with free radicals in the mitochondria can have a profound effect on the quality of life in old age.  At least if you are a mouse…

Stronger Muscles, Better Old Age

Everyone knows that as you get older, your body slowly starts to break down. For example, your muscles can weaken as you age and this can have profound consequences in terms of falling and loss of independence. Something like 30-50% of 80 year olds suffer from age-related muscle weakness.

Obviously it would be a boon to an aging population if we could somehow prevent this from happening. And this is apparently what happened when the mitochondria in mice were protected from damage. The protected mice suffered from less muscle weakness, were more willing to exercise and were generally stronger than their unprotected litter mates.

So if we can figure out how to safely and effectively get antioxidants to our mitochondria, we may end up living longer and healthier lives. Sure beats the idea of protecting our mitochondria by starving ourselves!