Evidence reveals that a link between aging and increased ROS production, accumulated oxidative damages and declined mitochondrial function.
Although aging is almost universally conserved among all organisms, the underlying molecular mechanisms of aging remain largely elusive. Many theories of aging have been proposed, including the free-radical and mitochondrial theories of aging. Both theories speculate that cumulative damage to mitochondria and mitochondrial DNA (mtDNA) caused by reactive oxygen species (ROS) is one of the causes of aging.
ROS (reactive oxygen species), at low level under normal conditions, is found to act as signaling molecules in many physiological processes, including redox homeostasis and cellular signal transduction. By activating proteins such as tyrosine kinases, mitogen-activated protein kinases, or Ras proteins, ROS are important mediators of signal transduction pathways.
Dependent on cell types, ROS have been found to function as signaling molecules in cell proliferation, cellular senescence, or cell death.The divergent effects of ROS on many cellular processes suggest that ROS are not merely detrimental byproducts, but also generated purposefully to mediate a variety of signaling pathways.
Oxidative damage affects replication and transcription of mtDNA and results in a decline in mitochondrial function which in turn leads to enhanced ROS production and further damage to mtDNA.