Some biochemical parameters of ageing in relation to dietary protein

De, Ajit; Chipalkatti, S.; Aiyar, A. S.

doi:10.1016/0047-6374(83)90014-3

Cited by 45 publications

(16 citation statements)

References 35 publications

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“…Females may have derived greater benefit because they do not grow as large (see Promislow 1993), because they are otherwise burdened with greater reproductive costs (see Graves 1993), or because of some differential intervention by the sex hormones. Youngman et a1 (1992) confirmed that accumulation of protein damage was offset by either caloric or protein restriction (see also Barrows and Kokkonen 1975;Fernandes et al 1976;Stoltzner 1977;Goodrick 1978;De et al 1983;Morse et al 1985). Decreased longevity with a high-protein diet (Table 5) was associated with accelerated FR damage (Tables 1 and 3).…”

Section: Impact Of Dietsmentioning

confidence: 65%

Accelerated aging of giant transgenic mice is associated with elevated free radical processes

Rollo¹,

Carlson²,

Sawada³

1996

Can. J. Zool.

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Transgenic growth hormone mice lived half as long as normal on a 23% protein diet. Longevities of both transgenic and control mice on a 38% protein diet were half those on 23% protein food. We hypothesized that transgenic mice are energetically constrained by their rapid growth, so energy supplements might improve "longevity assurance investments." As predicted, sucrose supplements extended the longevity of transgenic females (from a mean of 3 15 to 4 19 d). We measured two key biomarkers of aging (in brain, heart, liver, musculature, and kidneys) to test whether aging of these mice conformed to the free radical theory. Transgenic mice showed elevated levels of both superoxide radical (SOR) and lipid peroxidation (LP) compared with controls. The pattern of SOR and LP levels across kinds of mice and diets supported a free radical interpretation of aging and suggested that energy supply (protein or sugar) may impact longevity. The brain and heart were key biomarkers of longevity. LP levels in either organ explained 89% of the variation in longevity associated with genotype, sex, and diet. If combined with dietary restriction, this system should yield an 8-fold range in longevity, representing a powerful new tool for research into life histories and gerontology.RCsumC : Les souris transgkniques quant 2i l'hormone de croissance vivent la moitiC moins longtemps que normalement lorsqu'elles sont soumises 2i un rCgime contenant 23% de protCines. La longCvitC des souris transgkniques et des souris tCmoins nourries 2i un regime contenant 38% de protCines Cquivaut 2i la moitiC de celle des souris nourries 2i un rCgime contenant 23% de protCines. Nous posons en hypothkse que les souris transgkniques subissent des contraintes CnergCtiques imposCes par leur croissance rapide et que des supplCments CnergCtiques pourraient amCliorer leurs investissements en vue d'une 1ongCvitC accrue. Tel que prCdit, des supplCments de sucrose ont entrain6 une amklioration de la longCvitC chez des femelles transgkniques (de 3 15 jours en moyenne 2i 419 jours). Nous avons mesurC deux importants marqueurs biotiques du vieillissement (dans le cerveau, le coeur, le foie, la musculature et les reins) de f a~o n 2i dCterminer si le vieillissement de ces souris est conforme 2i la thCorie des radicaux libres. Les souris transgkniques ont des concentrations plus ClevCes du radical superoxyde (SOR) et des taux plus ClevCs de peroxydation des lipides (LP) que les souris tCmoins. Les patterns de SOR et de LP chez les diffkrents types de souris soumis 2i divers rCgimes alimentaires appuient la thCorie des radicaux libres pour expliquer le vieillissement et indiquent que les apports CnergCtiques (protCines ou sucres) peuvent avoir un impact sur la 1ongCvitC. Le cerveau et le coeur sont des indicateurs biologiques importants de la 1ongCvitC. L'importance de LP dans les deux organes explique 89% de la variation de la 1ongCvitC reliCe au genotype, au sexe et au rCgime alimentaire. CombinC 2i des restrictions alimentaires, ce systkme peut permettre une Ctendue d...

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Section: Impact Of Dietsmentioning

confidence: 65%

Accelerated aging of giant transgenic mice is associated with elevated free radical processes

Rollo¹,

Carlson²,

Sawada³

1996

Can. J. Zool.

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“…Thus, a decrease in lipid peroxidation and lipoxidation-derived protein damage has been reported in tissues (liver, heart, and brain) from CR rats and mice Laganiere and Yu 1987;Pamplona et al 2002a, b, c;Yu 2005;Sanz et al 2005aSanz et al , b, 2006aAyala et al 2007;Gómez et al 2007;Naudí et al 2007;Caro et al 2008). CR has also been shown to reduce levels of lipofuscin in tissues of rodents and C. elegans (Enesco and Kruk 1981;De et al 1983;Rao et al 1990;Terman and Brunk 2004;Gerstbrein et al 2005;Hulbert et al 2007). No data are available for DNA damaged by carbonyl compounds.…”

Section: Membrane Unsaturation From a Dietary Restriction Approachmentioning

confidence: 95%

An evolutionary comparative scan for longevity-related oxidative stress resistance mechanisms in homeotherms

Pamplona

Barja

2011

Biogerontology

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Key mechanisms relating oxidative stress to longevity from an interespecies comparative approach are reviewed. Long-lived animal species show low rates of reactive oxygen species (ROS) generation and oxidative damage at their mitochondria. Comparative physiology also shows that the specific compositional pattern of tissue macromolecules (proteins, lipids and nucleic acids) in long-lived animal species gives them an intrinsically high resistance to modification that likely contributes to their superior longevity. This is obtained in the case of lipids by decreasing the degree of fatty acid unsaturation, and in the case of proteins by lowering their methionine content. These findings are also substantiated from a phylogenomic approach. Nutritional or/and pharmacological interventions focused to modify some of these molecular traits were translated with modifications in animal longevity. It is proposed that natural selection tends to decrease the mitochondrial ROS generation and to increase the molecular resistance to the oxidative damage in long-lived species.

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“…[74][75][76][77][78][79][80][81][82][83][84] CR has also been shown to reduce levels of lipofuscin in tissues of rodents and C. elegans. [62,[85][86][87][88] From these studies it can be inferred that the magnitude of the change is modest for membrane unsaturation (between 2.5-10%) than that for the lipoxidation-derived molecular damage (between 20-40%) likely due to the added effect of the lower mitochondrial free radical generation also induced by these nutritional interventions. In addition to the moderate but significant effect on membrane unsaturation, these nutritional interventions show an effect that is directly related to the percent of the dietary restriction applied, being both protein and methionine restriction (80% MetR) even more intense and effective that caloric restriction.…”

Section: Mechanism Responsible For the Longevity-related Differences mentioning

confidence: 98%

Regulation of Membrane Unsaturation as Antioxidant Adaptive Mechanism in Long-lived Animal Species

Naudí

Jové

Ayala

et al. 2011

Free Radicals and Antioxidants

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Oxidative stress resulting from biomolecular oxidative damage due to the imbalance between reactive species production and antioxidant response has become an universal constraint of life-history evolution in animals and a modulator of phenotypic development and trade-offs. Redox balance is an important selective pressure faced by most organisms, and a myriad of mechanisms have evolved to regulate and adjust this balance. This diversity of mechanisms means that organisms have a great deal of flexibility in how they deal with reactive species challenges across time, conditions, and tissue types, as well as that different organisms may evolve different strategies for dealing with similar challenges. In the following paragraphs, we review the adaption of biological membranes as structural antioxidant defense against reactive species evolved by animals. In particular, it is our goal to describe the physiological mechanisms underlying the structural adaption of cellular membranes to oxidative stress, to explain the meaning of this adaptive mechanism, and to review the state of the art about the link between membrane composition and longevity of animal species.

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Some biochemical parameters of ageing in relation to dietary protein

Cited by 45 publications

References 35 publications

Accelerated aging of giant transgenic mice is associated with elevated free radical processes

Accelerated aging of giant transgenic mice is associated with elevated free radical processes

An evolutionary comparative scan for longevity-related oxidative stress resistance mechanisms in homeotherms

Regulation of Membrane Unsaturation as Antioxidant Adaptive Mechanism in Long-lived Animal Species

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