There is currently a great deal of interest in examining the possibility that diet may play a role in minimizing mitochondrial damage. Studies indicate that supplementing the diet with antioxidants can protect against the age-related decline in mitochondrial function. A team of researchers at the University of Valencia, Spain, recently found that sulfur-containing antioxidants in the diet, as well as common dietary antioxidants like vitamins C and E, reduced damage to mouse mitochondrial DNA and helped preserve the naturally occurring, sulfur-containing mitochondrial antioxidant glutathione.
Scientists have noted that animals fed diets in which calories have been cut by as much as 40% live longer, so long as vital nutrients are supplied in adequate amounts. The goal in these experiments is to achieve “undernutrition without malnutrition.”
Why does caloric restriction prevent mitochondrial damage? Scientists are still debating the issue. Possibly mitochondrial oxygen use is minimized by a very-low-calorie diet. This means fewer damaging oxidants are produced.
In a recent article published in the American Journal of Physiology, researchers found even deeper effects of dietary control. Caloric restriction, it appears, changes the activity of genes. The mitochondria of liver cells taken from aging mice, they found, showed a marked stress response, and most age-related, stress-induced genetic alterations were either completely or partially prevented by caloric restriction.