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The explanation was that a restricted diet would not give enough material for the electron transport chain in the mitochondria to function fully. With fewer electrons to pass, there were also fewer oxygen free radicals produced. Aging, thus, slows down (Nelson).
Proponents of the free radical theory, however, believe that dietary antioxidants are not directly beneficial, as they do not reach mitochondrial DNA (Nelson 2000). The site remains vulnerable and susceptible to attack. However, supplemental antioxidants can indirectly increase lifespan by protecting other cell parts, like cellular proteins and membranes, from injury by free radicals. They still serve a valuable purpose in slowing aging down. The application of the free radicals theory has not reached perfection. Genetic change in achieving increased life span remains controversial and difficult to perform. Dietary restriction is un-attractive to most people and dietary antioxidants do not directly increase life span as they do not access mtDNA. But increased knowledge and understanding of the production, action and role of free radicals will help in the search for more effective, practical and attractive approaches to repairing the radical damage created by mtDNA (Nelson).
Chronic or unmanageable fatigue is another link between mitochondrial malfunction and aging. It is a chronic condition, which is not corrected or allayed by sleep or rest (Nicolson 2003). Fatigue is defined as a multi-component sensation, which relates to aging and reduced mitochondrial function and loss of ability to produce high-energy molecules for cell functions. Certain natural foods and supplements are believed to reduce oxidative injury and replace absent high-energy molecules or repair mitochondrial malfunction. These supplements can reduce fatigue as well. Experiments showed that mitochondrial function in aging respondents was restored in comparable young adults who likewise experienced fatigue when they ate the supplements. The anti-aging and anti-fatigue properties of the foods protect mitochondria and cells from oxidative damage (Nicolson).
Respiratory, coronary, skeletal-muscular and bowel disorders, cancers and infections are often accompanied by chronic fatigue (Nicolson 2003). It often presents itself as an important secondary clinical symptom in many disorders. Although it has yet to be completely understood, fatigue involves a loss of energy and the inability to perform even easy and simple tasks without unduly draining oneself. Studies on aging respondents sought to determine their responses to certain foods. It has been established that damage to cellular mitochondria can affect the production of high-energy molecules. This is observed to accompany aging when substantial damage to mitochondrial molecules occurs. The production of ROS during aging can bring on oxidative stress and injury to the cell. This, in turn, oxidizes lipids, proteins or enzymes and the cell's DNA. When this happens, cellular molecules are deactivated or changed structurally or functionally. Most of the damage occurs at the mitochondria and the nuclei. This damage extends to membrane lipids and protein enzymes. DNA is either deleted or changed. ROS is produced and damage to mitochondria and nuclei happen through a lifetime but natural cellular systems neutralize and fetter out excess ROS and repair the damage it wreaks. In aging, ROS damage is accumulated and exceeds the neutralizing capability of the cell to repair or replace alterations and molecular damage within the cell. This also occurs in disease conditions (Nicolson).
Fatigue and aging seem linked. A decrease in energy production with aging is associated at least partly with mitochondrial lipid peroxidation by ROS and the body's failure to replace or repair the injured molecules. Damage to the membranes and the consequent dysfunction of mitochondria by ROS can also lead to certain changes, such as mutations and deletions in the mitochondrial DNA or mtDNA. The mitochondrial theory of aging suggests that degenerative disease is explained partly by accumulated mtDNA mutations and deletions and oxidative injury to mitochondrial members through time. These findings connected chronic diseases to the degree of mitochondrial membrane lipid peroxidation and mtDNA injury. This is why experts link or relate the damage of mtDNA and mitochondrial membrane age-related degenerative diseases. These diseases lead to important cell changes, which determine its survival and say a lot about the disturbing phenomenon known as aging (Nicolson).
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