Their experiments focused on ‘switching on’ these genes, restoring the glycine levels in the cells and reviving the mitochondria – reversing respiratory ageing.
In the study report published in Nature’s Scientific Reports, the authors suggest that elderly people could take glycine supplements to achieve a similar effect.
The best way for elderly people to keep their mitochondria healthy is to exercise and not eat too much, according to Professor Jun-Ichi Hayashi of the University of Tsukuba, who led the research.
But he warned that people must be careful before taking extra glycine, pointing to a recent report that showed it ‘possibly enhances cancer cell proliferation’.
Have you ever wondered how long you’re going to live? The potential answer can be found in the energy-producing cellular powerhouses called mitochondria.
According to a growing number of cell biologists, the number and functionality of the mitochondria specifically determine an individual’s life span.
When we’re young, we are relatively protected against mitochondrial deterioration. As we age, however, changes within our cells lead to the destruction of mitochondria—paving the way for aging and disease.
Unfortunately, a byproduct of this energy generation is the formation of a huge stream of free radicals.Free radicals are molecules that possess a free electron—a property that makes them react with other molecules in volatile and highly destructive ways.
Free radicals attack the structure of our cell membranes, creating metabolic waste products that disturb DNA and RNA production, interfere with the synthesis of protein, and destroy important cellular enzymes. Vital tissues and molecules decay under the assaults of free radicals. In addition, free-radical disruption of cell mechanics creates mutant cells, which are linked to cancer and cellular aging.
Mitochondria are the easiest targets of free-radical injury for two reasons:
- They are located exactlywhere these free radicals are produced, and
- They lack most of the antioxidant defenses found in other parts of the cell.
Evidence strongly indicates that over time, accumulated damage to the DNA of the mitochondria in particular leads directly to metabolic disorders (such as diabetes) and degenerative disorders (such as Alzheimer’s).
Mitochondrial dysfunction is primarily seen in organs and tissues that have a high demand for energy—explaining why cardiovascular tissue and brain neurons are among the most susceptible.
When we’re young, we are largely protected against mitochondrial deterioration because our bodies produce substances to defend mitochondria from the onslaught of free radicals. However, as we age, that protection wanes, setting us up for a destructive cycle that accelerates aging and disease. As a result of this rapidly accelerating process, mitochondria in the cells of elderly people are mostly dysfunctional, whereas young individuals have virtually no mitochondrial damage.