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Cellular changes
Damaged protein levels increase. Protein turnover declines. DNA damage
Somatic DNA accumulates mutation. Mitochondrial DNA damage.
Telomere shortening. Lipofuscin deposits in cells. Mitochondria function declines. Gene expression changes.
Response to cellular stresses.
Mitochondrial DNA damage is more extensive and persists longerthan nuclear DNA damage in human cells following oxidative stress
A significant amount of reactive oxygen species (ROS) is generated during mitochondrial oxidative phosphorylation. Several studies have suggested that mtDNA may accumulate more oxidative DNA damage relative to nuclear DNA. A model is presented in which chronic ROS exposure, found in several degenerative diseases associated with aging, leads to decreased mitochondrial function, increased mitochondrialgenerated ROS, and persistent mitochondrial DNA damage. Thus persistent mitochondrial DNA damage may serve as a useful biomarker for ROSassociated diseases.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC19544/pdf/pq000514.pdf
Schematic representation of the role of mitochondria in the generation of ROS and oxidative stress
Protein turnover
Progressive decrease in the creation of new protein. Reduction in the rate of protein degradation. Inaccessible protein deposits. Result: damaged proteins in cells increase as we age
A decline in fractional muscle mitochondrial protein synthesis occurred with age. Approximately a 40 percent decline occurred by middle age (P < 0.01), but there was no further decline with advancing age. ** Indicates significant difference from young age. Source: Rooyackers et al., 1996
http://www.chm.bris.ac.uk/webprojects2002/rakotomalala/maillard.htm