Mitochondrial Point Mutations Contribute to Female Reproductive Aging, and NAD+ Upregulation Attenuates These Consequences in Mice

Today's open access paper discusses the impact of mitochondrial DNA damage on female reproductive capabilities. Mitochondria are the power plants of the cell, a herd of hundreds of organelles responsible for packaging the chemical energy store molecule ATP, used to power cellular processes. They are additionally deeply integrated into many core cellular processes. Mitochondria are the evolved descendants of ancient symbiotic bacteria: they carry their own small genome, the mitochondrial DNA, and replicate like bacteria. Unfortunately this mitochondrial DNA is more vulnerable and less proficiently repaired than the nuclear DNA in the cell nucleus, and it accumulates mutational damage. Most is washed out by cell turnover in the body, but this damage nonetheless adds up over a lifetime. Some rare forms of mitochondrial DNA mutation, such as large deletions, can give rise to dysfunctional mitochondria that overtake their cells. The cell itself becomes dysfunction, exporting damaging reactive molecules into the surrounding tissue. This happens infrequently, but is sufficiently problematic when it does occur for it to contribute to aging. Other forms of mitochondrial mutation, such as point mutations, can also be a problem via a more subtle degradation of mitochondrial function. Mutator mice that accumulate this form of damage much more rapidly than their peers exhibit accelerated age-related degeneration, however. This is driven by the progressively greater dysfunction of m...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs