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Irvine, Calif. In the Jan. The cellular energy is used for two purposes: to generate heat to maintain our body temperature and to synthesize ATP adenosine triphosphate , a chemical form of energy that permits us to do work such as exercise, think, write, and make and repair cells and tissues.

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The mtDNAs are the blue prints for our mitochondrial power plants and determine the proportion of the calories in our diet that are allocated to generate body heat versus work. According to Douglas C.

Wallace, the Donald Bren Professor of Biological Sciences and Molecular Medicine at UCI and one of the co-authors of the report, after early humans migrated to colder climates, their chances of survival increased when mutations in their mtDNA resulted in greater body heat production during the extreme cold of the northern winters.

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The mtDNA mutations made it possible for individuals to survive the winter, reproduce and colonize the higher latitudes. It also explains why people with a certain ancestral history may be more susceptible to some diseases.

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Thus, our genetic history is linked to our current diseases, resulting in the new field of evolutionary medicine. One link would be the production of oxygen radicals in cells.

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  • Created when mitochondria burn our dietary fuel, this by-product can be responsible for damaging and killing cells, leading to several age-related diseases. Hence these people are less prone to aging and age-related degenerative diseases.

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    When mitochondria burn our dietary fuel, they generate a toxic by-product called oxygen radicals, the mitochondrial equivalent to the smoke generated by coal-burning power plants. Oxygen radicals damage the mitochondria, mtDNA and the surrounding cell. Eventually oxygen radicals can cause the cell to die when sufficient oxidative damage accumulates in the mitochondria and the cell.

    Since many of the tissues of our bodies have a finite number of cells, when sufficient cells die organs malfunction, resulting in the symptoms of age-related degenerative diseases and aging.

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    If all the calories that an individual consumes are used in generating carbon dioxide, water and energy, little fuel is left over to generate the oxygen radicals; however, if more calories are consumed than are needed to make energy, then these excess calories are stored as fat and drive a chronic increase in mitochondrial oxygen radical production. Consider two individuals that eat the same number of calories and get the same amount of exercise.

    The individual with a mtDNA mutant that increases heat production will require more calories for energy production and thus will have fewer calories left over to produce oxygen radicals. This individual will be partially protected from age-related diseases and will live longer. By contrast, the individual with mitochondria that make more ATP per calorie burned will store fat and generate more oxygen radicals if he or she eats the same level of calories as the individual with the cold-adapted mitochondria.

    About the University of California, Irvine: The University of California, Irvine is a top-ranked public university dedicated to research, scholarship and community. Founded in , UCI is among the fastest-growing University of California campuses, with more than 23, undergraduate and graduate students and about 1, faculty members. Materials provided by University Of California - Irvine.

    Note: Content may be edited for style and length. Science News. How mtDNA control the production of oxygen radicals When mitochondria burn our dietary fuel, they generate a toxic by-product called oxygen radicals, the mitochondrial equivalent to the smoke generated by coal-burning power plants.

    ScienceDaily, 14 January University Of California - Irvine. Retrieved June 25, from www. They consume between and g per day. The reason behind this habit, which Below are relevant articles that may interest you.

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