Especially those synthesized int the cellular mitochondria

Aug 6, 2009 14:30 GMT  ·  By

Scientists at the prestigious Swedish medical university the Karolinska Institutet have recently made an astounding find related the phenomenon of premature aging, which has thus far eluded plausible explanations. The experts managed to trace the origins of this condition to proteins that malfunction when they are synthesized in the cell's power plants, the mitochondria. When errors occur in their creation, they begin behaving erratically, and start impeding cell respiration, the process that allows cells to extract energy from nutrients. When this happens, cells start to age faster, AlphaGalileo reports.

The new groundbreaking study could be used to gain a deeper knowledge on how mitochondria work, and also on the conditions that need to be met before proteins start falling apart. The same phenomenon occurs when a person gets old. Eventually, cellular respiration becomes impeded, and the cells die. The new study was focused on determining the cause of premature aging, and not of that caused by old age. According to researchers, impeded cell respiration can easily lead to conditions ranging from a wide variety of genetic conditions to diabetes, cancer, Parkinson's disease and the normal aging process.

Mitochondrial “installations” inside the cell play perhaps the most important role of any cells inside the body. Through their actions, they convert, for example, the oxygen in the blood carried from the lungs to each cell into a form of energy that the body can use, known as the ATP (adenosine triphosphate) molecules. As soon as impairments appear in ATP generation, the body is essentially deprived of its vital energy, and begins to fall apart, cell by cell. That is why it is extremely difficult to find a cure for old age, as experts need to address tens of problems at the same time, not just one.

The KI group has recently proven in a study on innocent mice that changes in mitochondrial DNA (mtDNA) have the ability to cause rapid aging, on account of the fact that they introduce multiple changes in the protein production process. Despite the fact that the proteins appear to be normal, they are in fact unstable, and quickly disintegrate, triggering a cascade of chemical reactions that eventually stops cellular respiration and kills the cell.

“Our results show that premature aging is caused by point mutations in the mtDNA, which cause the mitochondrial proteins to become unstable and disintegrate,” sums up researcher Aleksandra Trifunovic, one of the leading experts of the new study. A paper accompanying the find, entitled “Random Point Mutations with Major Effects on Protein-Coding Genes Are the Driving Force behind Premature Aging in mtDNA Mutator Mice,” appears in the August 6 issue of the respected scientific journal Cell Metabolism.