Mitochondria are the power plants of the cell, known to be important in aging. They have their own DNA, inherited from the mother, and genetic variations lead to different levels of mitochondrial efficiency. This DNA becomes damaged in the course of aging, and in recent years researchers have been investigating ways to replace mitochondria and their DNA, the basis for therapies to treat this contribution to degenerative aging.
Of related interest, researchers here show that mitochondrial DNA variations impact heart disease risk. This is another incentive to complete the development of technologies that will allow replacement of mitochondrial DNA with some more optimal form, not just to repair damage that occurs over a lifetime.
"Having been in this field for decades, I remember when mitochondrial DNA variations were thought to play a role only in the rarest of genetic syndromes. Today, there is a growing consensus that variations in mitochondrial DNA alone make a substantial contribution to each person's risk for heart disease, and ours is the first study to directly confirm it in a living mammal."
The research team started with two varieties of mice; the C57 mouse known to be vulnerable to diseases associated with diet, and the C3H mouse, which is resistant. The study authors then used a technique called nuclear transfer to remove the nucleus from an embryo in each mouse line and switch them. Because mitochondria reside in the cytoplasm (not in the switched nuclei), the new embryos grew into mice whose cells had their own mitochondrial DNA and the nuclear DNA from the other line. That enabled researchers to compare mice with the same nuclear DNA, but different mitochondrial DNA, isolating the latter's distinct contribution to risk.
In general, the data showed that replacing mitochondrial DNA alone could increase or decrease a given mouse's susceptibility to a model of heart failure. Mice with efficient C57 mitochondrial DNA also generated 200 percent more oxidants than their disease-resistant counterparts with C3H mitochondrial DNA.
Another study underway [is] comparing mitochondrial DNA variations in people of African versus northern European ancestry. Evidence suggests that mitochondria carrying African mitochondrial DNA get more energy from the same amount of oxygen and sugar, perhaps reflecting an evolutionary history of food scarcity. Early migrating humans may have found more food in Europe, but would also have had to brave the cold. Thus, Euro mitochondria appear to be less efficient, perhaps because a byproduct of such inefficiency is the increased generation of body heat. More efficient mitochondria, with their greater oxidant production, may explain, in part, higher incidents of heart disease and diabetes among those of African ancestry in the face of modern, high-calorie diets.