Dual staining of PCNA and phosphorylated H2AX in a cell encountering DNA replication stress

 Xiahong Helena Yang, in Lee Zou laboratory


 There's no scientific reason that we know about why aging cannot be cured, and in that sense it's not different from cancer.

— Jan Vijg

DNA Damage and Repair

MOST BIOLOGICAL THEORIES of aging assume that DNA damage is centrally involved in aging in some way. DNA damage is widely thought to be the result of oxidative stress — exposure to oxygen radicals — as a consequence of cellular metabolic functions, although other factors, such as exposure to radiation, are thought to play a role. Failure of cellular DNA repair mechanisms is usually assumed to be the major factor in cellular aging. The major questions in this research area are whether DNA damage is, in fact, the primary cause of aging at the cellular level, whether cellular aging is relevant to aging of whole organisms, whether DNA damage can be prevented with anti-oxidants or other treatments, and whether DNA repair failure can be prevented in some way. Mitochondria are tiny organelles found in the cells of all eukaryotes (organisms with true nuclei that divide by mitosis). These organelles, thought to have been free-living bacteria in the early days of evolution, now supply about 90 percent of the metabolic energy used by multi-cellular creatures, combining foods with oxygen to produce spendable energy in the form of ATP. Their role in oxygen metabolism makes them prime targets for DNA damage from oxygen radicals. Research on the effects of oxygen radical damage on mitochondrial DNA (mtDNA) is a very active part of the aging research arena.

See also: Mitochondria and Aging

 

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