Protein oxidation associated with aging is reduced by dietary restriction of protein or calories.

Abstract

The accumulation of unrepaired oxidative damage products may be a major factor in cellular aging. Both oxidative lesions in DNA and oxidatively damaged proteins have been shown to accumulate during aging. The accumulation of oxidized proteins in Fischer 344 rats was compared for animals consuming protein-restricted and calorically restricted diets-both of which have been shown to extend lifespan. Rats were fed diets restricted in either protein (5% or 10% ofthe diet as compared with the normal 20% casein), or calories (25% or 40% less than normal), or total diet (40% less than normal). In addition, some of the rats fed a diet providing 5% or 20% protein were irradiated twice weekly (125 rads per exposure; 1 rad = 0.01 Gy). The level of oxidative damage to proteins (protein carbonyls) was determined in rats sacrificed at various times. The oxidative damage to proteins increased with aging and with radiation. Either protein or calorie restriction markedly inhibited the accumulation of oxidatively damaged proteins. Protein restriction reduced the accumulation of oxidatively damaged proteins during the oxidative stress of chronic irradiation.

Effect of exercise and calorie restriction on biomarkers of aging in mice

“…Studies examining differences in protein carbonyls with short-or long-term exercise and/or calorie restriction have been mixed with some documenting a significant reduc- tion (25,43,44), while others have observed no significant effect of treatment (15,35). It is possible that the lack of differences in carbonyls from this study was due to the age of the animals (12 and 36 wk old), which likely have greater capacity for protein turnover than older mice.…”

Dietary fat composition influences glomerular and proximal convoluted tubule cell structure and autophagic processes in kidneys from calorie-restricted mice

“…According to the ‘Mitochondrial Free Radical Theory of Aging’ (Miquel et al ., 1980), accumulation of reactive oxygen species (ROS) in mitochondria (the subcellular organelle with the highest rate of ROS production) results in damage not only to mitochondrial DNA and proteins, but also to membrane phospholipids, and this oxidative damage is decreased in animals maintained on CR (Youngman et al ., 1992; Pamplona et al ., 2002). An inverse correlation between lifespan and the degree of membrane phospholipid unsaturation has been proposed (Pamplona et al ., 2002; Hulbert, 2003), with PUFAs being more susceptible to peroxidation and other modifications which result in the accumulation of oxidative injury in membranes containing these fatty acids.…”

Artemisinin mimics calorie restriction to extend yeast lifespan via a dual-phase mode: a conclusion drawn from global transcriptome profiling

“…As an evolutionarily conserved character, CR-enhanced survival and longevity have been described in yeast [2], worms [3], fruit flies [4] and mammals [5]. In yeast, both the chronological lifespan (CLS) and the replicative lifespan (RLS) can be extended by reducing glucose from 2% to 0.5%.…”