Effect of caloric restriction on mitochondrial reactive oxygen species production and bioenergetics: reversal by insulin

Lambert, Adrian J.; Merry, B.J.

doi:10.1152/ajpregu.00341.2003

Cited by 102 publications

(81 citation statements)

References 46 publications

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“…However, when animals are subjected to short-term CR (Ͻ6 mo), a reduction or no change has been reported depending on the study (15,25,41). In our 3-mo CR assessment, we did not find a statistically significant reduction in H 2 O 2 production, although females showed a trend toward a reduction (P ϭ 0.08), achieving levels similar to that in males.…”

Section: Sexual Dimorphism In Liver Mitochondriamentioning

confidence: 54%

Sexual dimorphism in liver mitochondrial oxidative capacity is conserved under caloric restriction conditions

Valle¹,

Guevara²,

García-Palmer³

et al. 2007

American Journal of Physiology-Cell Physiology

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Valle A, Guevara R, García-Palmer FJ, Roca P, Oliver J. Sexual dimorphism in liver mitochondrial oxidative capacity is conserved under caloric restriction conditions. Am J Physiol Cell Physiol 293: C1302-C1308, 2007. First published July 25, 2007; doi:10.1152/ajpcell.00203.2007.-Caloric restriction (CR) without malnutrition has been shown to increase maximal life span and delay the rate of aging in a wide range of species. It has been proposed that reduction in energy expenditure and oxidative damage may explain the life-extending effect of CR. Sex-related differences also have been shown to influence longevity and energy expenditure in many mammalian species. The aim of the present study was to determine the sex-related differences in rat liver mitochondrial machinery, bioenergetics, and oxidative balance in response to short-term CR. Mitochondria were isolated from 6-mo-old male and female Wistar rats fed ad libitum or subjected to 40% CR for 3 mo. Mitochondrial O 2 consumption, activities of the oxidative phosphorylation system (complexes I, III, IV, and V), antioxidative activities [MnSOD, glutathione peroxidase (GPx)], mitochondrial DNA and protein content, mitochondrial H 2O2 production, and markers of oxidative damage, as well as cytochrome C oxidase and mitochondrial transcription factor A levels, were measured. Female rats showed a higher oxidative capacity and GPx activity than males. This sexual dimorphism was not modified by CR. Restricted rats showed slightly increased oxygen consumption, complex III activity, and GPx antioxidant activity together with lower levels of oxidative damage. In conclusion, the sexual dimorphism in liver mitochondrial oxidative capacity was unaffected by CR, with females showing higher mitochondrial functionality and ROS protection than males.

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Section: Sexual Dimorphism In Liver Mitochondriamentioning

confidence: 54%

Sexual dimorphism in liver mitochondrial oxidative capacity is conserved under caloric restriction conditions

Valle¹,

Guevara²,

García-Palmer³

et al. 2007

American Journal of Physiology-Cell Physiology

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“…The finding that mild uncoupling, like CR, enhances both forms of life span suggests this may be a viable intervention to prevent aging in more complex organisms. Indeed, CR has been shown to promote a decrease in protonmotive force and ROS release in rats (36). Furthermore, individual mice with longer life spans have larger respiratory rates and proton leaks (37), supporting the idea that CR causes mild uncoupling that is responsible for the prevention of aging.…”

Section: Discussionmentioning

confidence: 91%

Higher Respiratory Activity Decreases Mitochondrial Reactive Oxygen Release and Increases Life Span in Saccharomyces cerevisiae

Barros

Bandy

Tahara

et al. 2004

Journal of Biological Chemistry

301

237

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Increased replicative longevity in Saccharomyces cerevisiae because of calorie restriction has been linked to enhanced mitochondrial respiratory activity. Here we have further investigated how mitochondrial respiration affects yeast life span. We found that calorie restriction by growth in low glucose increased respiration but decreased mitochondrial reactive oxygen species production relative to oxygen consumption. Calorie restriction also enhanced chronological life span. The beneficial effects of calorie restriction on mitochondrial respiration, reactive oxygen species release, and replicative and chronological life span could be mimicked by uncoupling agents such as dinitrophenol. Conversely, chronological life span decreased in cells treated with antimycin (which strongly increases mitochondrial reactive oxygen species generation) or in yeast mutants null for mitochondrial superoxide dismutase (which removes superoxide radicals) and for RTG2 (which participates in retrograde feedback signaling between mitochondria and the nucleus). These results suggest that yeast aging is linked to changes in mitochondrial metabolism and oxidative stress and that mild mitochondrial uncoupling can increase both chronological and replicative life span.The only intervention known to increase average and maximum life span in mammals is caloric restriction (CR), 1 a reduction of 25-60% in calorie intake without essential nutrient deficiency. This diet not only extends life span but also delays many unwanted effects of aging and age-related pathologies. CR is highly effective in a wide range of organisms, increasing life span by up to 50% in some species (reviewed in Refs. 1-3). Unfortunately, the mechanisms through which it results in increased life span are still controversial (see Ref. 4 for a critical review).A leading hypothesis on the mechanism through which CR prevents aging is that this process decreases reactive oxygen species (ROS) generation and, hence, the oxidation of cellular components (5-8). Indeed, aging is usually accompanied by oxidative damage of DNA, proteins, and lipids (9, 10). CR promotes a metabolic shift resulting in more efficient electron transport in the mitochondrial respiratory chain (1, 5). Faster and more efficient electron transport may lead to lower production of ROS by mitochondria, one of the major intracellular ROS sources. This occurs because of reduced leakage of electrons from the respiratory chain and/or lower oxygen concentrations in the mitochondrial microenvironment (11,12). Indeed, artificially increasing mitochondrial respiration using uncouplers such as 2,4-dinitrophenol (DNP) strongly prevents mitochondrial ROS release (11). Furthermore, CR decreases ROS release/O 2 consumed in isolated mammalian mitochondria (13), possibly because of enhanced expression of mitochondrial uncoupling proteins (14,15). Despite this evidence supporting a correlation between ROS-induced damage and aging, a clear cause-effect relationship has been hard to establish, and conflicting results are often p...

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“…Similarly, lens epithelial cells isolated from CR mice are resistant to H 2 O 2 -induced cell death (Li et al, 1997) and show enhanced proliferative capacity, though only for a short time when isolated using standard cell culture techniques (Li et al, 1998). Further, CR in rats reduces the production of reactive oxygen species (ROS) from liver mitochondria in vivo (Lambert and Merry, 2004); however this difference is not maintained in hepatocyte cultures derived from these same animals (Lambert and Merry, 2005). There is some data to suggest that serum from rodents exposed to a CR diet can increase the stress resistance of cell lines in vitro (de Cabo et al, 2003;Cohen et al, 2004), but such systemic factors cannot be involved in our own system, in which both control and experimental cell lines are maintained in identical culture conditions through multiple weeks, using fetal bovine serum as a source of growth factors.…”

Section: Discussionmentioning

confidence: 99%

Stress resistance and aging: Influence of genes and nutrition

Harper

Salmon

Chang

et al. 2006

Mechanisms of Ageing and Development

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Previous studies have shown that dermal fibroblast cell lines derived from young adult mice of the long-lived Snell dwarf (dw/dw), Ames dwarf (df/df) and growth hormone receptor knockout (GHR-KO) mouse stocks are resistant, in vitro, to the cytotoxic effects of hydrogen peroxide, cadmium, ultraviolet light, paraquat, and heat. Here we show that, in contrast, fibroblasts from mice on low-calorie (CR) or low methionine (Meth-R) diets are not stress resistant in culture, despite the longevity induced by both dietary regimes. A second approach, involving induction of liver cell death in live animals using acetaminophen (APAP), documented hepatotoxin resistance in the CR and Meth-R mice, but dw/dw and GHR-KO mutant mice were not resistant to this agent, and were in fact more susceptible than littermate controls to the toxic effects of APAP. These data thus suggest that while resistance to stress is a common characteristic of experimental life span extension in mice, the cell types showing resistance may differ among the various models of delayed or decelerated aging.

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Effect of caloric restriction on mitochondrial reactive oxygen species production and bioenergetics: reversal by insulin

Cited by 102 publications

References 46 publications

Sexual dimorphism in liver mitochondrial oxidative capacity is conserved under caloric restriction conditions

Sexual dimorphism in liver mitochondrial oxidative capacity is conserved under caloric restriction conditions

Higher Respiratory Activity Decreases Mitochondrial Reactive Oxygen Release and Increases Life Span in Saccharomyces cerevisiae

Stress resistance and aging: Influence of genes and nutrition

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