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Calorie restriction reduces production of reactive oxygen species (ROS).[69][87] ROS cause several types of DNA damage including 8-hydroxy-2’-deoxyguanosine (8-OHdG). The level of 8-OHdG is often used as an indicator of the general level of oxidative damage in DNA. Sohal et al. observed that caloric restriction decreased 8-OHdG damages in the DNA of mouse, heart, skeletal muscle, brain, liver and kidney. The levels of 8-OHdG in the DNA of these organs in 15 month old mice were reduced to an average of 81% of that in the DNA of mice fed an unrestricted diet.[88] Kaneko et al. observed that, in rats, dietary restriction retarded the onset of age-related increases in 8-OHdG in nuclear DNA of brain, heart, liver and kidney. The level of 8-OHdG in these organs of the calorie restricted rats at 30 months averaged 65% of the level in rats fed an unrestricted diet.[89] Hamilton et al. found that dietary restriction in both mice and rats reduced the age-related levels of 8-OHdG. In rats aged 24–26 months that had been fed a calorie restricted diet, the level of 8-OHdG in heart, skeletal muscle, brain and kidney DNA was, on average, 62% of the level in rats fed an unrestricted diet. In mice, after a calorie restricted diet for 24–26 months, the level of 8-OHdG in heart, brain, liver and kidney DNA averaged 71% of the level in mice fed an unrestricted diet.[90] Also, Wolf et al. observed that, in the rat, calorie restriction reduced 8-OHdG in the DNA of heart, skeletal muscle, brain and liver. After 24 months, the levels of 8-OHdG in these organs averaged 64% of those in the rats fed an unrestricted diet.[91] Thus in rodents, calorie restriction slows aging, decreases ROS production and reduces the accumulation of oxidative DNA damage in multiple organs. These results link reduced oxidative DNA damage to slower aging. The consistent observation that calorie restriction reduces oxidative DNA damage lends support to the proposal of Holmes et al. that oxidative DNA damages are a prominent cause of aging.[71] This is also discussed in detail by Bernstein et al.[92] |
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