It is natural that all living beings age. As a human being matures, there are numerous changes that take place within the body which influences the effectiveness of the cells. A significant feature of this change is referred to as mitochondrial dysfunction. The mitochondria are small organelles within our cells.
They can be referred to as the powerhouses of the cell as they generate most of energy that the cells require to survive. The malfunction of mitochondria may influence the functioning of the whole body. This essay will describe the relationship between mitochondrial dysfunction and aging, the state of science concerning this relationship, and its importance to our health.
Mitochondria are present in virtually all of the cells in the body. Their primary activity is to create a molecule known as ATP (adenosine triphosphate) that helps to supply energy in most of the cellular processes. The lack of sufficient ATP prevents the cells to complete various vital activities, including DNA repair, cell division, and the elimination of waste.
Mitochondria also play a role in the regulation of cell death, calcium levels and generation of reactive oxygen species (ROS) which are substances capable of causing damage to cells unless controlled. It has been found out that older people have less efficient mitochondria in producing ATP and more prone to producing ROS, resulting in cell and tissue damage.
The free radical theory is one of the oldest aging theories which were proposed in the 1950s. This theory holds that an aging process occurs due to damage of free radicals which are unstable molecules that are capable of injuring the proteins, DNA, and cell membranes.
Mitochondria are the origins as well as targets of free radicals. Damaged mitochondria produce more ROS that in turn results in more destruction in a vicious cycle. This idea is supported by numerous studies which showed that older animals and humans possess an increased amount of mitochondrial DNA damage and oxidative stress.
The DNA on the mitochondria (mtDNA) is distinct and does not relate to the DNA on the nucleus of the cell. The holding of the nuclear DNA, the mitochondrial DNA does not possess powerful shields and fix mechanisms. This exposes it to more susceptibility to ROS. The mutation in the mtDNA is built up over time and leads to the inefficiency of mitochondria in functioning.
A 2005 study by Wallace and associates, showed that the level of mutations of the mitochondrial DNA with age is positively associated with diminished efficiency and energy generation of the mitochondria. This implies that the development of the accumulation of the damage of mitDNA could be a prime characteristic of aging.
The tissues are also specifically affected by mitochondrial dysfunction. Mitochondrial diseases are more sensitive to age in organs that are sensitive to energy such as the brain, heart, and muscles. As an example, neurodegenerative diseases such as Alzheimer, Parkinson are associated with reduced energy production and an elevation in oxidative stress in the brain.
Mitochondrial deterioration in muscles plays a role in sarcopenia, the loss of muscle mass and muscle strength in old age. This is the reason why most elderly people get weak, tired, and their movement becomes slow with age.
The second factor is the case of mitochondrial role in cellular aging events like cellular senescence. Senescence is a condition where cells cease to divide releasing damaging substances that lead to inflammations and tissue destruction.
It has been demonstrated that senescence could be triggered by dysfunctional mitochondria. The less preserved the mitochondria the more cells tend to get into this deleterious condition resulting in aging and age-related illness.
The communication of mitochondria with other parts of the cell is also under study. This is referred to as mitochondrial signaling. Due to the stress or dysfunction of mitochondria, they provide signals that may alter the behavior of the cell.
Other signals have the capability of engaging repair pathways, whereas others can trigger inflammatory or cell death pathways. It is known that chronic stimulation of these stress signals is a cause of aging and most diseases.
Since the mitochondria are involved in aging to this extent, scientists are considering the possibilities of enhancing mitochondrial activity to prevent disease and slow aging. One of these fields is concerned with exercise.
Exercise has been found to accelerate mitochondrial biogenesis, or formation of new mitochondria, and mitochondrial efficiency. This is part of the reason why exercising is known to be linked with good health and low aging.
The other topic of interest is diet and caloric restriction. Animal experiments demonstrated that caloric restriction in the absence of malnutrition was capable of enhancing the quality of mitochondria and lifespan.
Scientists believe that this occurs due to the fact that caloric restriction lowers the metabolic stress and ROS generation which enables the mitochondria to be more efficient at their job. Certain antioxidants, nutrients, and compounds, including coenzyme Q10, resveratrol, and some others are also under investigation to help support the well being of mitochondria.
Nevertheless, not everything has been obvious. Although antioxidants appear to be a promising theory, numerous clinical trials on humans have failed to reveal a definite advantage of slowing down age or prolonging life.
This implies that aging is a complicated process and the minimizing of ROS may not be sufficient. Probably, it can be more productive to address the health of mitochondria, such as better energy production and mitochondrial damage.
Scientists hope to come up with treatment that would directly target the mitochondria in the future. They may be gene therapies to fix the mitDNA, drugs which help the mitochondria to work better or treatments which destroy the damaged mitochondria and will be replaced with the healthy ones.
A small amount of research in animals has been encouraging, but there is still a lot that needs to be done before these techniques can be popular in humans.
Finally, a dominant element of the aging process is the dysfunction of the mitochondria. The older a person gets, the less energy and more harmful molecules are produced by mitochondria, thus causing cell damage, inflammation, and age-related deterioration.
The role of mitochondria in aging is useful in assisting scientists discover methods of staying healthy and extending life span. Although there is no means of preventing aging, one of the possible significant steps to make aging healthier is to enhance the way mitochondria work.
