02 December 2013

Be careful with antioxidants

Supplements with antioxidants: potential harm to the body's own defenses

NanoNewsNet based on the materials of the University of Oslo: Vitamins in a box: Can damage the body's own defenses"We believe that antioxidants benefit us because they protect cells from oxidative stress, which can harm our genes.

However, our body has a huge innate ability to cope with stress. The results of recent studies show that the body's response to stress really plays an important role in preventing DNA damage. I'm afraid that if we supplement our diet with vitamins, the delicate balance in our cells may be disrupted," says Hilde Nilsen, who heads a research group at the University of Oslo Biotechnology Center.


Hilde Nielsen. Photo: Ola SaetherOur DNA–the genetic code that makes us who we are–is constantly exposed to damaging factors.

In each of the hundred trillion cells of our body, up to two hundred thousand DNA-damaging events occur daily. They may be associated with environmental factors such as smoking, stress, pathogens or UV radiation, but the main source of DNA damage is the natural processes necessary for life that take place in the body itself.

How can DNA repair help us live long and stay healthy?

To answer this question, Hilde Nielsen and her group conducted a series of experiments on a small organism – Caenorhabditis elegans – a roundworm 1 millimeter long. The lifespan of C.elegans is only 25 days, but the genome of this animal, containing 20,000 genes, is surprisingly complex: we humans have the most by a couple of thousand genes.

C.elegans is a fantastically powerful research tool because scientists have learned how to change its hereditary properties. They can, for example, increase the worm's ability to repair its DNA or completely suppress it. In addition, they can observe what happens if DNA damage is not eliminated on several hundred organisms throughout their lives. Different types of DNA damage are dealt with by various "repair proteins", or, more scientifically, so-called repair proteins.

In some worms unable to repair their DNA, Nielsen and her colleagues observed a significant acceleration of the aging process. Most scientists explain this phenomenon by the accumulation of damage that prevents the synthesis of proteins necessary for the normal functioning of cells. But Nielsen calls these ideas into question.

One of the mutants studied by Norwegian researchers had a slightly shorter life span: he lived three days less than the usual C. elegans. Translated into human, this means death at the age of 60, not 70 years.

"We were surprised to see that these mutants do not actually accumulate DNA damage, which could be attributed to accelerated aging. On the contrary, their DNA is less damaged. This is because the little nematode slows down metabolism and turns on its own antioxidant defense. Nature uses this strategy to minimize the negative consequences of its inability to repair DNA. So why is this condition not normal? Most likely, because you have to pay a high price for it: such organisms have less ability to respond to stress – they are very vulnerable," says Nielsen.

She and her colleagues showed for the first time that this reaction of the body – slowing down metabolism and turning on antioxidant protection – is under active genetic control and is not caused, as is commonly believed, by the passive accumulation of DNA damage.

"This makes it possible to manipulate these processes. And that's exactly what we did – we restored the normal lifespan of a short-lived mutant by removing other proteins that repair damage. Therefore, the cause cannot be the accumulation of damage, since there is no reason to believe that a mutant deprived of alternative ways to restore its DNA will be less susceptible to them. There must be something else here," Nilsson continues.

The researchers concluded that this "something else" is actually other-leftover–repair proteins. They believe that by triggering a cascade of signals reprogramming the cell, these proteins prevent the occurrence of damage that they, "playing in an incomplete composition," will not be able to eliminate.

We must remember that, most likely, the purpose of DNA repair is to guarantee the reproduction of healthy offspring, and not at all the longest possible life after the end of the reproductive period. Initiating a survival-oriented reaction that enhances antioxidant protection means that the lack of the ability to repair DNA has less impact on our reproduction than it could. For the species as a whole, the loss by several individuals of the ability to cope well with stress and a shorter life expectancy is a small price.

Since this is an active cellular process, researchers consider it reprogramming.

"We found several trigger proteins for this reprogramming. This process has the same effect as reducing the caloric content of food, which is known to help increase the life expectancy of animals of many species. In other words, there are two paths to a long life. Simultaneous stimulation of both of these pathways increases the lifespan of our nematode by four times," says Nielsen.

The balance between oxidants and antioxidants is crucial for our physiology, but this balance is individual for each person.

"This is where synthetic antioxidants start to bother me. The cells of our body use this delicate balance to create the best possible conditions for themselves, and this adaptation is individual for each of us. Taking supplements with antioxidants, such as vitamins C and E, we can disrupt this balance," the scientist warns.

Nielsen emphatically states: "The fact that taking substances that prevent the accumulation of damage benefits us intuitively sounds right, and that is why so many of us supplement our diet with vitamins. The results of our research show that at the same time we can cause ourselves enormous harm. Instead, medicine recommends choosing a reasonable diet. I totally agree with that. It's much safer to get vitamins from food than from pills."

Portal "Eternal youth" http://vechnayamolodost.ru02.12.2013

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