A mutation in that gene can increase longevity. Experiments suggest that the increase in longevity with the daf mutations is due to an increased ability to resist oxidative damage. Professors Sun and Tower of the University of Southern California have demonstrated that fruit flies with overexpression of catalase, an enzyme that neutralizes some of the damaging reactive oxygen species produced in oxidative damage, are resistant to some of the deleterious effects of hydrogen peroxide, but live no longer than other fruit flies. As in other animal models, oxidative damage is reduced in mice under conditions of calorie restriction. Caloric restriction in mice has been demonstrated to reduce the destruction of nerve cells.
Thiamine deficiency is a condition that produces nerve damage through oxidative damage.
The researchers suggest that these results confirm the value of the mouse model in understanding the relationship between aging, oxidative damage and calorie restriction. They have monkeys in their study population that range up to 23 years old, and some of them have been subjected to calorie-restricted diets for as long as 10 years. The scientists have done skeletal muscle biopsies on the freely fed monkeys and compared them to biopsies on calorie-restricted monkeys. Levels of oxidative damage in skeletal muscle rose fourfold with aging in the freely fed monkeys, but the amount of observable oxidative damage was significantly less in the calorie-restricted monkeys.