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Philanthropy For Basic Science:
DNA & Mitochondrial Damage 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.
| "We believe that mitochondrial DNA damage is a major factor in aging, and that the cause of damage is the mitochondria generating oxygen radicals, which then attack their mitochondrial DNA" - Douglas Wallace | | | |
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.
Articles related to DNA & Mitochondrial Damage Probing Tiny Powerhouses
Geneticist Douglas Wallace is laying the groundwork for a whole new biomedical discipline: evolutionary medicine. For the past four decades, since his doctoral work at Yale University, Dr. Wallace has been probing the deep intricacies of tiny rod-like bodies — mitochondria — that reside by the dozens or hundreds inside every cell in the body.
Related Projects Phillip Carpenter, PhD
The University of Texas — Houston Medical School
New Scholar in Aging 1999
Biochemical Characterization of a Putative p53-Binding Protein from Xenopus | Bruce N. Ames, PhD
Children's Hospital of Oakland Research Institute
Senior Scholar in Aging 1999
Reversal of Mitochondrial Decay: From Rats to Humans | Douglas C. Wallace, Ph.D
Emory University, then University of California at Irvine
Senior Scholar in Aging 1999
Mitochondrial Aging in the Chimpanzee | James E. Cleaver, PhD
University of California at San Francisco, UCSF Cancer Center
Senior Scholar in Aging 1999
Endogenous DNA Damage and Mechanisms of Aging | Lawrence A. Loeb, MD, PhD
University of Washington
Senior Scholar in Aging 1999
Aging in Mutator and Antimutator Mice | David S. Thaler, PhD
The Rockefeller University
Senior Scholar in Aging 1999
Mitochondrial Mutation and Aging | James E. Sligh, MD, PhD
Vanderbilt University School of Medicine
New Scholar in Aging 2000
Altered Mitochondrial Function in Transgenic Models of Cutaneous Aging | Giuseppe Attardi, MD
California Institute of Technology
Senior Scholar in Aging 2000
Aging-Dependent Large Accumulation of Mutations at Specific Sites in Human Mitochondrial DNA Control Region | Philip C. Hanawalt, PhD
Stanford University School of Medicine
Senior Scholar in Aging 2000
Repair of Oxidative DNA Damage in Human Neurons | Simon Melov, PhD
Buck Institute for Age Research
Senior Scholar in Aging 2001
Critically Testing the Free Radical Theory of Aging, and Development of a Practical Intervention | Yidong Bai, PhD
The University of Texas Health Center at San Antonio
New Scholar in Aging 2002
Genetic and Functional Analysis of Mitochondrial DNA Mutations Associated with Aging |
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