The study, published in this Friday's issue of Science magazine, finds that accumulation of mitochondrial mutations that promote apoptosis, or programmed cell death, may be a central mechanism driving aging and may be unrelated to the release of free radicals, previously thought to cause aging. This may be because of an accumulation of DNA mutations in the mitochondria, the cellular powerhouse that converts food to energy.
Results from the study may lead to more effective methods to prevent aging and stress the importance of a healthy lifestyle, said Christiaan Leeuwenburgh, an associate professor in the department of aging and geriatric research in the College of Medicine and contributing author of the study. He estimated that average maximum human lifespan could be increased from the current 70 years to more than 100 years with exercise and a proper diet.
"All the therapies have been targeted to reduce the free radical production in the mitochondria, and now it looks like that doesn't make complete sense," he said.
By breeding mice with the inability to detect and repair mistakes in the DNA replication process, researchers discovered there was no increase in oxidative stress despite an increased mutational load. However, there was a significant increase in apoptosis, said Leeuwenburgh.
In mammals, uncorrected mistakes can cause genetic disorders, aging or even death, said doctoral student Asimina Hiona, who was instrumental in the biochemical analysis of free radicals and apoptosis in the study. In the mutated mice, that ability was impaired so the cells could not repair themselves.
The finding disproves the previously believed mitochondrial "vicious cycle" theory of aging, which states that in
Contact: Christiaan Leeuwenburgh
University of Florida