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You are here: Biology of Aging >

Mechanisms of Aging: Mitochondrial Burnout

The mitochondria are cellular power stations responsible for producing the majority of energy in the cell. All key processes in the cell depend on mitochondria feeding energy to the rest of the system. Unfortunately, the mitochondria are also responsible for the majority of free radical damage in the cells because most free radicals are by-products of mitochondrial fuel cycle. Since free radical damage and decreased energy production are the hallmarks of aging, mitochondria are believed to play one of the key roles in the aging process.

Since mitochondria are so important, cells have each many copies of mitochondria. Furthermore, mitochondria can make copies of themselves via division as well as repair some of the damage they suffer from free radicals. Yet, the mitochondria have unique vulnerabilities and design flaws, which arguably make them the weakest link in the cellular anti-aging defense.

Take DNA, for example. DNA damage is a major part of the aging process because, among other things, part of it is irreversible. Some DNA lesions get repaired, but others, once inflicted, become permanent. There are two compartments in the cell that contain DNA: the nucleus and the mitochondria. The nucleus contains most of the cell's genetic material packed into chromosomes. The mitochondria contain a small but indispensable portion of cellular DNA. As it turns out, free radical damage to DNA is much greater in mitochondria than in the nucleus. The DNA from mitochondria can suffer up to 10 times more damage than nuclear DNA. In part, this is because most free radicals are formed in mitochondria where the fuel is burned. Also, mitochondrial DNA is not as well protected by proteins and repair systems as nuclear DNA.

In time, energy producing capacity of mitochondria declines. It appears that mitochondria are the first cellular system to degenerate with age. This process is sometimes called mitochondrial burnout. As a result, cells become less metabolically active, which leads to the decreased functional capacity of organs, poor adaptability and progression of degenerative diseases.

Stress appears to be a major accelerator of the burnout of mitochondria. Stress increases energy demands, making mitochondria work harder, and leading to more oxidative by-products -- more free radicals. In a prolonged or intensive stress, mitochondrial membranes get so damaged by free radicals that they begin to leak, which disrupts the cells entire energy and chemical balance. The resulting disproportionately severe oxidative damage accelerates aging and promotes disease.

The key role of mitochondria as power stations and their particular susceptibility to free radical damage makes them an important potential target for anti-aging and anti-stress intervention. In fact, inhibiting mitochondrial burnout is one of the most promising avenues of life extension research. Several important nutrients were shown to be active in mitochondria and improve mitochondrial function: acetyl-L-carnitine (ALC), coenzyme Q10 (CoQ10) and R-alpha lipoic acid (R-ALA).

ALC is a part of the mechanism for the transport of fatty acids into the mitochondria. Although it can be synthesized in the body, the rate of its synthesis decreases with age. Supplementation with ALC speeds up the utilization of fats by mitochondria, improving energy production. Studies have shown ALC to be beneficial in some diseases of cardiovascular and nervous systems.

CoQ10 has two important roles: it is an essential part of the mitochondrial fuel cycle and it is an antioxidant. CoQ10 improves both the rate and efficiency of energy production and at the same time protects mitochondria from free radicals. The body can produce CoQ10, but many factors, including age, illness, cholesterol-lowering drugs and malnutrition can impair that ability. CoQ10 is sometimes called a biomarker of aging because its level correlates so well with aging and degenerative diseases. In some studies, CoQ10 supplementation modestly increased life expectancy of laboratory animals. A large number of human studies clearly demonstrated the effectiveness of CoQ10 in congestive heart failure and other diseases of heart muscle. Other conditions that appear to be helped by CoQ10 include hypertension, decreased immunity, and muscular atrophy.

Like CoQ10, R-alpha lipoic acid is both an important participant in the mitochondrial energy production and an antioxidant. In some studies, R-ALA acid supplementation lowered free radical levels in mitochondria and improved energy production.

Unfortunately, even though ALC, CoQ10 and R-ALA show some promise in protecting and revitalizing the mitochondria in some situations, more research is needed to determine if these or any other agents can actually slow down the mitochondrial burnout in the long run.


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