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1
المؤلفون: Brian J. Merry, Malcolm H. Goyns, Austin J. Kirk
المصدر: Mechanisms of Ageing and Development. 129:341-348
مصطلحات موضوعية: Male, Senescence, Aging, Time Factors, Antioxidant, medicine.medical_treatment, Longevity, Biology, chemistry.chemical_compound, Life Expectancy, Animal science, medicine, Animals, Dietary supplementation, Restricted diet, Models, Statistical, Thioctic Acid, Life span, Animal Feed, Rats, Lipoic acid, Feeding regime, Biochemistry, chemistry, Dietary history, Dietary Supplements, lipids (amino acids, peptides, and proteins), Energy Intake, Food Deprivation, Developmental Biology
الوصف: Dietary restriction feeding extends survival in a range of species but a detailed understanding of the underlying mechanism is lacking. There is interest therefore in identifying a more targeted approach to replicate this effect on survival. We report that in rats dietary supplementation with alpha-lipoic acid, has markedly differing effects on lifetime survival depending upon the dietary history of the animal. When animals are switched from DR feeding to ad libitum feeding with a diet supplemented with alpha-lipoic acid, the extended survival characteristic of DR feeding is maintained, even though the animals show accelerated growth. Conversely, switching from ad libitum feeding a diet supplemented with alpha-lipoic acid to DR feeding of the non-supplemented diet, blocks the normal effect of DR to extend survival, even after cessation of lipoic acid supplementation. Unlike the dynamic effect of switching between DR and ad libitum feeding with a non-supplemented diet where the subsequent survival trajectory is determined by the new feeding regime, lipoic acid fixes the survival trajectory to that established by the initial feeding regime. Ad libitum feeding a diet supplemented with lipoic acid can therefore act as mimetic of DR to extend survival.
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2
المؤلفون: Byung Pal Yu
المصدر: Mechanisms of Ageing and Development. 126:1003-1010
مصطلحات موضوعية: Senescence, Aging, medicine.medical_specialty, Free Radicals, Calorie restriction, Inflammation, Oxidative phosphorylation, Mitochondrion, Biology, medicine.disease_cause, Lipid peroxidation, chemistry.chemical_compound, Internal medicine, medicine, Animals, Humans, Caloric Restriction, Aldehydes, Cell Membrane, Lipids, Mitochondria, Cell biology, Oxygen, Oxidative Stress, Endocrinology, chemistry, Ageing, Lipid Peroxidation, medicine.symptom, Energy Intake, Energy Metabolism, Reactive Oxygen Species, Oxidation-Reduction, Oxidative stress, Developmental Biology
الوصف: As has been experimentally determined, oxidative modification to biological systems can be extensive, although the identification and stochiometric relation of the reactive species that cause these alterations have not been fully elucidated. In this review, arguments are presented to support the notion that the combined effects of membrane lipid peroxidation and its by-products, reactive aldehydes are likely responsible for membrane-associated functional declines during aging. As evidence for a systemic response to overall oxidative stress, the molecular inflammation hypothesis of aging is discussed by considering that the activation of inflammatory genes act as a bridge linking normal aging to pathological processes.
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3
المصدر: Mechanisms of Ageing and Development. 125:529-538
مصطلحات موضوعية: Glycation End Products, Advanced, Male, Senescence, Lipid Peroxides, Aging, medicine.medical_specialty, Blotting, Western, Glutamic Acid, Mitochondria, Liver, Oxidative phosphorylation, Mitochondrion, Biology, medicine.disease_cause, Gas Chromatography-Mass Spectrometry, Membrane Lipids, chemistry.chemical_compound, Rats, Inbred BN, Internal medicine, medicine, Animals, chemistry.chemical_classification, Fatty Acids, Proteins, Fatty acid, Malondialdehyde, Rats, Oxidative Stress, Endocrinology, chemistry, Ageing, Energy Intake, Oxidative stress, Developmental Biology, Polyunsaturated fatty acid
الوصف: To gain insight into the anti-ageing mechanisms of caloric restriction (CR), liver mitochondria were isolated from male Brown-Norway rats of different ages (fully fed control and CR) and various specific markers of non-enzymatic protein modification (by oxidative, glyco- and lipoxidative-reactions) were measured by GC/MS and Western blotting. A membrane peroxidizability index (PI) was calculated from the fatty acid profiles. Between 6 and 18 months of age, there were significant decreases in the concentration of all markers of damage in mitochondria from both the fully fed and CR groups. In contrast, between the ages of 18 and 28 months, there were significant increases in the concentrations of all markers of damage. In mitochondria from both fully fed and CR groups, there were significant increases in N-epsilon (Nepsilon)-(carboxymethyl)lysine (CML) and N-epsilon-(malondialdehyde)lysine (MDAL) between 6 and 28 months of age. In general, damage tended to be lower in mitochondria from CR animals, but the effects were not significant, except for the concentration of N-epsilon-(carboxymethyl)lysine at 28 months of age. PI increased steadily and significantly with age in fully fed animals, whilst CR induced a significant decrease in this index at 28 months of age. It is concluded that for male rats of the Brown-Norway strain, and mitochondria from liver (i) old (but not mature) age is associated with an increased membrane PI and protein oxidative damage and (ii) CR does not lead to a general reversion in age-related protein damage, but it does prevent the age-induced increase in PI very late in life.
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4
المؤلفون: Tomas A. Prolla, Cheol Koo Lee, Tsuyoshi Kayo, Richard Weindruch
المصدر: Mechanisms of Ageing and Development. 123:177-193
مصطلحات موضوعية: Male, Senescence, Aging, Transcription, Genetic, Macromolecular Substances, Gene Expression, Biology, Mice, chemistry.chemical_compound, Transcription (biology), Gene expression, medicine, Animals, Muscle, Skeletal, Gene, Oligonucleotide Array Sequence Analysis, Gene Expression Profiling, Brain, Proteins, Skeletal muscle, Molecular biology, Cell biology, Mice, Inbred C57BL, Gene expression profiling, medicine.anatomical_structure, chemistry, DNA microarray, Energy Intake, DNA, Developmental Biology
الوصف: We have previously employed high density oligonucleotide arrays representing thousands of genes to determine the gene expression profile of the aging process in skeletal muscle (gastrocnemius) and brain (cerebellum and neocortex) of male C57BL/6 mice. Specific gene expression profiles are associated with the aging process of individual organs, and caloric restriction can prevent or retard the establishment of these gene expression alterations. The use of DNA microarrays may provide a new tool to measure biological age on a tissue-specific basis and to evaluate at the molecular level the efficacy of interventions designed to retard the aging process.
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5
المؤلفون: Joe Chehade, Arshag D. Mooradian
المصدر: Mechanisms of Ageing and Development. 115:101-106
مصطلحات موضوعية: Leptin, Male, Senescence, Aging, medicine.medical_specialty, Calorie, Endogeny, Fructose, Biology, chemistry.chemical_compound, Basal (phylogenetics), Dietary Sucrose, Hyperinsulinism, Internal medicine, medicine, Hyperinsulinemia, Animals, Osmolar Concentration, medicine.disease, Obesity, Rats, Inbred F344, Rats, Glucose, Endocrinology, chemistry, Energy Intake, Developmental Biology
الوصف: To determine if aging is associated with altered serum leptin response to diet-induced changes in endogenous hyperinsulinemia, male Fisher 344 (F344) rats at different age groups were studied while on regular rat chow and following 10 days of experimental diets consisting of 60% of the weight as fructose or glucose. The serum leptin concentration (ng/ml) gradually increased from basal levels of 2.5+/-0.1 at age of 4 months to 3.7+/-0.1, 6.9+/-0.9, 9. 4+/-0.3 and 8.9+/-1.1 at 6, 12, 18 and 24 months of age, respectively (P0.001). Hyperinsulinemia associated with 60% fructose diet was associated with increased serum leptin levels in 4, 12, and 24 month old rats to 5.1+/-0.8, 6.7+/-1.2, and 8.6+/-1.1, respectively (P0.001). Feeding 60% glucose diet also was associated with increased serum leptin levels in 4, 12 and 24 month old rats to 7.6+/-0.6, 7.2+/-0.7, and 9.1+/-1.1, respectively (P0.001). Restricting dietary intake to 60% of the calories consumed by control rats for 10 days resulted in a decrease in serum leptin to 1.0+/-0.02 in 4 month old rats and 2.5+/-0.4 in 24 month old rats (P0.01). It is concluded that aging in F344 rats is associated with increased serum leptin concentrations. However, diet-related hyperinsulinemic effect on leptin is blunted in aging rats although leptin response to caloric restriction is maintained. The inability of aging rats to mount hyperleptinemic response to dietary changes may contribute to the age-related increase in adiposity.
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6
المؤلفون: Melanie Halbleib, Martin S. Obin, Abigail Pike, Allen Taylor, Ruth D. Lipman, Roderick T. Bronson
المصدر: Mechanisms of Ageing and Development. 114:133-147
مصطلحات موضوعية: Male, Senescence, Aging, medicine.medical_specialty, genetic structures, Calorie restriction, Cell Count, Biology, Retina, chemistry.chemical_compound, Rats, Inbred BN, Internal medicine, medicine, Animals, Outer nuclear layer, BROWN NORWAY, Retinal, Anatomy, eye diseases, Rats, medicine.anatomical_structure, Endocrinology, chemistry, Inner nuclear layer, sense organs, Neuron, Energy Intake, Developmental Biology
الوصف: The present study examined the effect of a 40% reduction in caloric intake (CR) versus ad libitum (AL) feeding on retinal aging. CR- and AL-fed Brown Norway (BN) rats were obtained at 12, 24 and 30 months of age from the National Center for Toxicological Research (NCTR). Age-dependent declines in outer nuclear layer (ONL=photoreceptor) cell densities, ONL height, inner nuclear layer (INL) cell densities, and thicknesses of the inner retina and whole retina were quantified in thick sections at six loci across the circumference of the sensory retina (four peripheral, two central). Data were analyzed by repeated measures, general linear models. Aging in both diet groups was associated with declines in ONL cell density, ONL height, peripheral INL cell density and total retinal thickness (Por =0.05). However, ONL cell densities, ONL height and retinal thickness were significantly greater in the CR versus AL diet group at all three ages (Por =0.005). CR was also associated with a trend for greater peripheral INL cell density (P=0.06) and with greater INL thickness at 30 months (Bonferroni P=0.03). Elevated ONL cell densities in the CR-12 cohort relative to the AL-12 cohort could be explained by diet-associated differences in retinal length, i.e. delayed retinal growth in response to CR. Enhanced ONL cell density, ONL height, INL cell density, INL thickness and total retinal thickness in the CR-30 cohort appear to be as a result of reduced rates of retinal cell loss between 24 and 30 months. However, the protective effect of CR in retinas of older animals may also reflect the initial growth-associated enhancements which were observed in 12 month-old animals. The rat retina may provide a useful model for elucidating the neuroprotective mechanism(s) of CR.
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7
المؤلفون: Casilda V. Mura, Jodi Dunning, Donald Smith, Xin Gong, Fu Shang, Mona M Scrofano, Maureen Kelliher, Thomas R. Nowell, Allen Taylor
المصدر: Mechanisms of Ageing and Development. 105:273-290
مصطلحات موضوعية: Male, Senescence, Aging, Ubiquitin-Protein Ligases, Calorie restriction, Endogeny, Lactoglobulins, Ubiquitin-conjugating enzyme, medicine.disease_cause, Substrate Specificity, Ligases, Mice, chemistry.chemical_compound, Adenosine Triphosphate, Ribonucleases, Ubiquitin, Paraquat, medicine, Animals, Ubiquitins, biology, Cell biology, Oxidative Stress, Liver, chemistry, Biochemistry, Ubiquitin-Conjugating Enzymes, biology.protein, Female, Rabbits, Energy Intake, Adenosine triphosphate, Oxidative stress, Developmental Biology
الوصف: Calorie restriction (R) is the only known method to delay the aging process and extend mean and maximal lifespan in rodents. R has been shown to delay the age-related accumulation of damaged proteins and to protect organisms from various stresses which can produce damaged proteins. Such stresses include irradiation, heat shock, and oxidative stress. The ubiquitin- and ATP-dependent proteolytic pathway (UPP) has been associated with the degradation of abnormal and/or damaged proteins. We examined the effect of diet and oxidative stress on activities of the UPP in supernatants from livers taken from 23-month-old Emory mice which had been exposed to an in-vivo injection of paraquat. Paraquat induces oxidative stress by generating superoxide radicals. In livers from non-stressed animals, steady-state levels of endogenous ubiquitin conjugates, de novo conjugate formation, and E1 and E2 activities were significantly lower in R animals than in control (C) animals. However, after exposure to paraquat, levels of endogenous ubiquitin conjugates were significantly higher in R versus C animals, and de novo conjugate formation and E1 and E2 activities in R animals rose to levels which were indistinguishable from levels of these activities noted in C animals. R was associated with an increased ability to degrade beta-lactoglobulin by the UPP after an oxidative stress was imposed. Ability to degrade beta-lactoglobulin by the C or R livers in non-stressed animals was not significantly different. Taken together, these data indicate that oxidative stress in R animals is associated with enhanced levels of ubiquitin conjugates and that this enhancement may be due to an increase in UPP activity. These data also indicate that the ability to form ubiquitin conjugates and the UPP system does not change with oxidative stress in C animals. The latter is consistent with prior reports that suggests that older C animals may already be in a state of enhanced oxidative stress and that activities of the UPP provide a sensitive indicator of levels of cellular redox status.
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8
المؤلفون: Keith R Martin, Ruth D. Lipman, Guohua Cao, Ronald L. Prior, Sung Nim Han, Dayong Wu, Mohsen Meydani, Roderick T. Bronson, D.E. Smith, Simin Nikbin Meydani
المصدر: Mechanisms of Ageing and Development. 103:269-284
مصطلحات موضوعية: Male, Vitamin, Aging, medicine.medical_specialty, medicine.medical_treatment, media_common.quotation_subject, Longevity, Biology, Antioxidants, Lesion, Melatonin, Mice, chemistry.chemical_compound, Internal medicine, medicine, Animals, Vitamin E, media_common, Plant Extracts, Incidence, Body Weight, Fatty liver, medicine.disease, Glutathione, Middle age, Mice, Inbred C57BL, Endocrinology, chemistry, Food, Fortified, Population study, Animal Nutritional Physiological Phenomena, medicine.symptom, Energy Intake, Developmental Biology, medicine.drug
الوصف: The ability of augmented antioxidant consumption to alter disease incidence, lesion burden and/or longevity was studied in adult male C57BL/6 mice. Mice were fed modified AIN76 diet or modified AIN76 supplemented with vitamin E, glutathione (GSH), vitamin E and GSH, melatonin or strawberry extract starting at 18 months of age. All the mice in this study were heavier than reference populations of male C57BL/6 mice fed NIH-07 or NIH-31, which were maintained without a mid-life change in diet. Fatty liver, focal kidney atrophy and proteinacious casts in the renal tubules were observed more frequently in this study population than in the reference populations. Lesion burden and incidence of specific lesions observed amongst the various groups in this study did not differ. There were no differences observed for longevity of any of the study groups. The longevity observed in this study was similar to that previously reported for male C57BL/6 mice. Thus, diet supplementation with antioxidants initiated during middle age did not appear to affect age-associated lesions patterns, lesion burden or longevity for ad libitum fed male C57BL/6 mice.
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9
المؤلفون: Bheemappa G. Devi, Makau Lee
المصدر: Mechanisms of Ageing and Development. 89:11-20
مصطلحات موضوعية: Male, Senescence, Aging, medicine.medical_specialty, Endogeny, Biology, medicine.disease_cause, Lesion, Random Allocation, chemistry.chemical_compound, Internal medicine, medicine, Animals, Aspirin, Ethanol, Stomach, Anti-Inflammatory Agents, Non-Steroidal, digestive, oral, and skin physiology, Glutathione, Rats, Inbred F344, Rats, medicine.anatomical_structure, Endocrinology, chemistry, Biochemistry, Gastric Mucosa, medicine.symptom, Energy Intake, Adenosine triphosphate, Oxidative stress, Developmental Biology, medicine.drug
الوصف: The present study was designed to determine whether dietary restriction would render rats more resistant to experimental gastric mucosal injury induced by either aspirin or acidified ethanol. We have found that dietary restriction rendered rats more resistant to experimental gastric mucosal injury, and that dietary restriction prevented decreases in endogenous mucosal antioxidants (such as glutathione) and energy stores (such as adenosine triphosphate) in rat stomachs that had been injured by acidified ethanol. Our findings suggest that dietary restriction may reverse some of the age-related reductions in gastric mucosal protective factors and thereby may render the aged stomach more resistant to experimental injury.
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10
المصدر: Mechanisms of Ageing and Development. 72:155-163
مصطلحات موضوعية: Senescence, Aging, medicine.medical_specialty, Thiobarbituric acid, Ratón, Linoleic acid, Longevity, Biology, Lipid peroxidation, Mice, chemistry.chemical_compound, Internal medicine, medicine, Animals, Mice, Inbred C3H, Autoxidation, Fatty Acids, Mice, Inbred C57BL, Endocrinology, Liver, chemistry, Docosahexaenoic acid, Microsomes, Liver, Microsome, Female, Lipid Peroxidation, Energy Intake, Food Deprivation, Developmental Biology
الوصف: Lipid peroxidation potential in hepatic microsomes from young and old mice following two different caloric restriction regimens was measured by a colorimetric thiobarbituric acid method under conditions where Fe2+ autoxidation and free oxygen redical production were undetectable. Peroxidation was highest in the young (3.5-month-old) slightly restricted group (caloric intake 75% of ad libitium mice) but very low in young severely restricted (caloric intake 50% of ad libitum mice) and in both old (27-month-old) slightly and severely restricted groups. Very old (45-month-old) severely restricted animals had intermediate lipid peroxidation potentials. Fatty acid composition of liver homogenates was also determined. Significant differences between groups were found for only three fatty acids. Linoleic acid (18:2(n-6)) decreased in aged slightly restricted animals while it remained stable in severely restricted animals during aging. Dihomo-gamma-linolenic acid (20:3(n-6)) was higher in very old restricted animals than in old slightly restricted animals. Docosahexaenoic acid (22:6(n-3)) decreased in old slightly restricted animals. These reuslts indicated that the effect of diets on hepatic fatty acid composition and the potential for microsomal lipid peroxidation in mice was dependent on the degree of caloric restriction and age.
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