Summary: Here’s what researchers have discovered about stopping the destruction caused by free radicals, including DNA damage, macromolecular damage, and damage to mitochondrial DNA. [This article first appeared on the website LongevityFacts.com. Author: Brady Hartman. ]
However, they may have found a way to stop it.
Free Radicals and DNA Damage
Free radicals are the principal cause of DNA damage, and our bodies generate them every minute in every one of our cells. Free radicals are members of a family known as reactive oxygen species (ROS). The ROS family includes free radicals, as well as other damaging molecules such as hydrogen peroxide.
Free Radical Theory Of Aging
The idea that free radicals cause aging was proposed by Leo Szilard in a 1959 paper, who argued that free radicals cause DNA damage. The free radical theory has been superseded by modern damage theories, such as the network theory of aging which goes hand-in-hand with the disposable soma theory of aging that proposes evolutionary forces are behind the aging process.
Szilard’s paper led to the current widespread view that DNA damage and other macromolecular damage are principal causes of aging for most animals. Szilard said this damage accumulated as the result of lifelong exposure to ionizing radiation as well as free radicals and other toxins.
When not repaired, this damage accumulates, leading to mutations in our nuclear DNA, mitochondrial DNA as well as our epigenome. The damage caused by ROS, toxins, injuries and other and other assaults is cumulative and causes disease, aging and probably even cancers.
High Rate of DNA Damage
This DNA damage occurs daily at a remarkable rate. Moreover, mistakes happen when our cells divide. At the same time, another type of damage occurs that needs to be repaired as well. The net result is that our cellular repair mechanisms get overwhelmed. The combined stresses cause breaks in our DNA. Each time a cell divides, it has about 50 breaks or so. Added to this are thousands of assaults that every cell receives every day of its existence.
The cell makes mistakes carrying out these repairs, introducing epigenetic alterations that can persist after the repairs are completed. The epigenome incurs changes called epimutations, as a result of DNA methylation, or modifications in histones, the spools around which DNA wind. As Jim Mellon and Al Chalabi (M+C), authors of the book, Juvenescence put it,
“aggregation of unrepaired DNA causes genome-wide epigenetic change over time,”
The authors go on to say that
“It is now thought by some eminent scientists that if the repair process of DNA could be enhanced, then the build-up of such epigenetic change could be reversed or at least slowed.”
Free Radicals and Mitochondria
We all need to breathe, and our mitochondria produce reactive oxygen species when they process oxygen. Our mitochondria carry out a process called aerobic respiration that sometimes produces partly-metabolized oxygen, the cause of free radicals. Free radicals, are molecules with unpaired electrons and cause damage by stealing electrons from their neighbors. These free radicals create a multitude of macromolecular damage, including damage to mitochondrial DNA (mtDNA), nuclear DNA and surrounding structures.
Researchers have long known that dysfunctional mitochondria cause aging. Free radicals cause damage to our mitochondrial DNA, which in turn causes ill health and accelerates the aging process. Scientists have known for some time that mitochondria play a role in cancer. Researchers also agree that damaged mitochondria contribute to the chronic conditions of aging, including type 2 diabetes, heart disease, Parkinson’s and Alzheimer’s disease.
Mitochondrial Dysfunction With Age
Mitochondrial dysfunction is one of the nine hallmarks of aging. As we get older, our mitochondria decline both in quality and quantity. Researchers suspect this decline is partially responsible for a general overall deterioration, including areas such as endurance, hearing, intellect, and lower muscle strength.
Not only does the quantity of our mitochondria decline as we age, but the remaining ones become less efficient and generate less energy while producing more toxic reactive oxygen species. As we age, our cell is making less anti-oxidant defenses. Free radicals are not a problem for young people whose bodies manufacture plenty of anti-oxidants, but as our defenses decline in old age, oxidative damage takes a toll on our cells.
Antioxidants and Free Radicals
The body has natural antioxidants that usually mop up free radicals before they do any damage. These antioxidants include superoxide dismutase (SOD), catalase, and glutathione peroxidase. As authors M+C put it,
“However, this chemical security force can and does fail to disarm all the free radicals that the cell makes. And it is because some ROS evade antioxidants that genetic mutations, damage to our lipids (fats) and damage to our proteins start to occur.”
When we are young, our bodies have plenty of these antioxidants and in the 1980’s and 1990’s proponents of the free radical theory of aging advocated taking antioxidant supplements to ward off the damage.
While the body’s natural antioxidant molecules quench free radicals, these aren’t the bad guys they were once portrayed to be. Free radicals have multiple roles within the cell, sometimes beneficial, at other times destructive. As M+C point out,
“Intriguingly, it is now pretty certain that many antioxidant supplements play no, or little, positive role in preventing this type of damage.”
Calorie Restriction Fights Free Radicals
Antioxidant supplements seem to offer little protection against damage from reactive oxygen species. M+C suggest that calorie restriction or intermittent fasting protects our bodies against these free radicals, saying
“calorie restriction (CR) is a mild positive stressor for our cells and seems to stimulate the body’s production of natural antioxidants. ”
Unfortunately, calorie restriction is hard for people to practice and that’s why researchers have come up with drugs that mimic its effects, most notably rapamycin. The drug doesn’t necessarily quench free radicals. However, research says it speeds up the cellular housekeeping service known as autophagy.
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Cover photo: Getty Images.
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