One of the highlights of postmitotic aging is the intracellular accumulation of highly oxidized and cross-linked proteins, known as lipofuscin. Lipofuscin is insoluble and not degradable by lysosomal enzymes or the proteasomal system, which is responsible for the recognition and degradation of misfolded and oxidatively damaged proteins. These aggregates have been found in various cell types, including heart, liver, kidney, neuronal tissue, and dermal tissue, and are associated with the life span of a single postmitotic cell and, consequently, of the whole organism. Lipofuscin formation appears to depend on the rate of oxidative damage to proteins, the functionality of mitochondrial repair systems, the proteasomal system, and the functionality and effectiveness of the lysosomes. This review highlights the current knowledge of the formation, distribution, and effects of lipofuscin in mammalian cells.
One of the hallmarks of chronic or severe oxidative stress is the accumulation of oxidized proteins, which tend to form high-molecular-weight aggregates. The major proteolytic system responsible for the removal of oxidized cytosolic and nuclear proteins is the proteasome. This complicated proteolytic system contains a core proteasomal form (20S proteasome) and several regulators. All of these components are affected by oxidative stress to various degrees. The ATP-stimulated 26S proteasome is sensitive to oxidative stress, whereas the 20S form seems to be more resistant. The nuclear proteasome selectively degrades oxidatively damaged histones in the nuclei of mammalian cells, where it is activated and regulated by automodified PARP-1 after oxidative challenge. In this brief review we highlight the proteolysis and its regulatory effects during oxidative stress.
The objective of the present study was to investigate the contribution of intra-individual variance of resting energy expenditure (REE) to interindividual variance in REE. REE was measured longitudinally in a sample of twenty-three healthy men using indirect calorimetry. Over a period of 2 months, two consecutive measurements were done in the whole group. In subgroups of seventeen and eleven subjects, three and four consecutive measurements were performed over a period of 6 months. Data analysis followed a standard protocol considering the last 15 min of each measurement period and alternatively an optimised protocol with strict inclusion criteria. Intra-individual variance in REE and body composition measurements (CV intra ) as well as interindividual variance (CV inter ) were calculated and compared with each other as well as with REE prediction from a population-specific formula. Mean CV intra for measured REE and fat-free mass (FFM) ranged from 5·0 to 5·6 % and from 1·3 to 1·6 %, respectively. CV intra did not change with the number of repeated measurements or the type of protocol (standard v. optimised protocol). CV inter for REE and REE adjusted for FFM (REE adj ) ranged from 12·1 to 16·1 % and from 10·4 to 13·6 %, respectively. We calculated total error to be 8 %. Variance in body composition (CV intra FFM) explains 19 % of the variability in REE adj , whereas the remaining 81 % is explained by the variability of the metabolic rate (CV intra REE). We conclude that CV intra of REE measurements was neither influenced by type of protocol for data analysis nor by the number of repeated measurements. About 20 % of the variance in REE adj is explained by variance in body composition.Resting energy expenditure: Intra-individual variance: Interindividual variance: Resting energy expenditure prediction Individuals vary in their resting energy expenditure (REE). The majority of interindividual variance in REE (CV inter ) is explained by fat-free mass (FFM), fat mass (FM), age and sex, leaving only 19 % unexplained (Ravussin et al. 1986). Unexplained variance is mainly due to composition of FFM, genetic factors and thyroid hormone levels (Müller et al. 2002). In comparison with CV inter , intraindividual variance in REE (CV intra ) is reported to be low (2-10 %; Soares & Shetty, 1986;Weststrate, 1993). However, CV intra could partly explain the interindividual variance in REE observed in different studies by contributing to between-group differences (i.e. between normal-weight and overweight subjects). Intra-individual variance in REE is explained by biological and methodological variability in REE. Since FFM is the major determinant of REE, the biological and methodological variance in FFM adds to the variance in REE adjusted for FFM. Intra-individual variance in REE may also contribute to inaccuracies of REE prediction by both limiting the accuracy of databases for the generation of prediction formulas as well as the implementation of such a formula on the individual level. Applying established REE prediction equa...
The objectives of the present study were to evaluate the effect of normobaric and hyperbaric O 2 (HBO) on plasma antioxidants and biomarkers of oxidative stress in plasma and urine and to investigate the effect of a 4-week vitamin C plus E supplementation on HBO-induced oxidative stress. Nineteen healthy men were exposed to HBO (100 % O 2 ; 240 kPa) before and after 4 weeks' supplementation with 500 mg vitamin C plus 165 mg a-tocopherol equivalents. Exposure to 21 % O 2 at 100 kPa served as intra-individual controls (control). Samples for the analysis of plasma antioxidants and oxidative stress biomarkers were collected before and immediately after each treatment. The present results showed that when compared with 'control', a single exposure to HBO resulted in a decrease of plasma vitamin C (P¼ 0·027) and an increase of lipid peroxides (P¼ 0·0008) and urinary 8-oxo-deoxyguanosine (8-oxodG) excretion (P¼ 0·006). Oxidative stress was not prevented by a 4-week supplementation with vitamins C and E. HBO-induced changes in plasma parameters correlated with basal antioxidant levels. The increase of urinary 8-oxodG after HBO plus supplementation correlated negatively with vitamin E intake (P¼ 0·023). We concluded that in healthy men HBO caused oxidative stress, which could not be prevented by dietary vitamin C plus E supplementation. The present data support the idea that HBO is a suitable model for oxidative stress in healthy volunteers.Hyperbaric oxygen: Normobaric oxygen: Oxidative stress: Supplementation: Vitamin C: Vitamin E The human organism is constantly exposed to oxidants (reactive oxygen species) from both physiological processes and pathophysiological conditions, foreign compound metabolism and radiation 1 . An increased production of reactive oxygen species together with a failure of the network of enzymic, endogenous and nutritional antioxidants leads to oxidative stress. Chronic oxidative stress may be involved in the development of chronic diseases such as cancer, CHD, neurodegenerative diseases, diabetes mellitus and cataract, and has also been suggested as a mechanism of ageing 2 . Therefore, maintaining the endogenous antioxidant defence system by supplementing with antioxidants appears worthwhile.However, current research results concerning the protective effects of antioxidants on biomarkers of oxidative stress and on diseases are contradictory 3 -11 . Several intervention studies showed some protective effects, while others did not. The results of a meta-analysis of nineteen randomised, placebo-controlled trials with high-dose vitamin E rather than dietary levels showed a dose-dependent relationship between vitamin E supplementation and all-cause mortality 12 . Specifically, all-cause mortality in volunteers with a high risk for a chronic disease progressively increased for dosages approximately greater than 100 mg/d.It has been suggested that a preventive effect of antioxidants may only be seen in a situation of high oxidative stress 13 and we therefore based the present study on the following ...
Aim: To investigate the effect of a 4-week vitamin C and E supplementation on oxidative stress induced by hyperbaric oxygen (HBO). Methods: 19 healthy men were exposed to 3 sequential protocols, i.e. HBO (100% O2, 2.4 bar, 131 min) before (T1) and after 4 weeks of daily supplementation with 500 mg slow-release vitamin C and 272 IU vitamin E (T2). A normoatmospheric protocol (21% O2, 1.0 bar, 131 min) served as control treatment (nonexposed). Blood samples were taken before (B) and immediately after (A) treatment. Plasma levels of vitamin A, C, E, β-carotene, reduced glutathione and malondialdehyde were measured by HPLC. Antioxidative capacity and lipid peroxides in plasma were analyzed by ELISA. Results: HBO decreased vitamin C and antioxidative capacity (T1). At T1, Δ A – B of vitamin C and lipid peroxides was different from nonexposed. Vitamin supplementation increased plasma levels of vitamin C and E by 28 and 37%, respectively. Vitamin supplementation led to decreased concentrations of lipid peroxides and reduced glutathione. After supplementation, HBO decreased vitamin C and reduced glutathione. At T2, Δ A – B of vitamin C and lipid peroxides was significantly different from nonexposed. Conclusion: In humans, oxidative stress decreased plasma levels of vitamin C and antioxidative capacity and increased plasma lipid peroxides. Supplementation with vitamin C and E did not prevent these effects.
ZusammenfassungDer Mensch verbraucht ständig Energie. Der tägliche oder 24−Stunden−Energieverbrauch (= 24−h−EE, 24 h energy expenditu− re) ist die Summe des Ruheenergieverbrauchs (= REE, resting energy expenditure), der für körperliche Aktivitäten aufzuwen− denden Energien (sog. arbeitsinduzierte Thermogenese, = AEE, activity energy expenditure) und der nahrungsinduzierten Ther− mogenese (DIT, diet−induced thermogenesis oder TEF, thermic ef− fect of food). Der REE erklärt 60 ± 70 % des 24−h−EE, die DIT beträgt 5 ± 10 %. Bei einem inaktiven Lebensstil erklärt die AEE 20 ± 30 % des 24−h−EE, das Verhältnis AEE/REE beträgt heute im Mittel der Bevölkerung etwa 0,5. Das Prinzip der Messungen geht auf den ersten Hauptsatz der Thermodynamik zurück, wonach in einem geschlossenen System Energie weder erzeugt noch vernichtet werden kann. Indirekte und direkte Kalorimetrie, Isotopendilu− tion, 24−Stunden−Herzfrequenzmessung und Bewegungsmesser sind für die Erfassung der verschiedenen Komponenten des Energieverbrauchs geeignet. Die intra− und interindividuellen Varianzen der verschiedenen Methoden zeigen erhebliche Un− terschiede (VKintra von 5 % für den REE bis zu 22,7 % für Bewe− gungsmessungen; VKinter von 4,5 % für Messungen des 24−h−EE in einer Respirationskammer bis zu 69,2 % für den AEE unter All− tagsbedingungen). Neben den technisch methodischen Vorraus− setzungen müssen bei der Wahl der Methoden die Zielgrößen, die Machbarkeit und die gewünschte Genauigkeit beachtet wer− den. Aufgrund der heute verfügbaren und an jeweils größeren Bevölkerungsgruppen erhobenen Messwerte wurden neue Prä− Abstract 24 hour energy expenditure (24h−EE) is the sum of resting ener− gy expenditure (REE), activity energy expenditure (AEE) and diet− or food−induced thermogenesis (DIT). REE explains 60 ± 70 % of 24h−EE, DIT is about 5 ± 10 %. AEE is highly variable. In a sendentary lifestyle AEE contributes to 20 ± 30 % of 24h−EE. Methods of assessment of energy expenditure follow the first law of thermodynamics and include direct and indirect calori− metry, isotope dilution techniques (ie doubly−labelled water or NaH 13 CO 2 −turnover), 24h−heart rate monitoring, and measure− ment of movement (eg accelerometry). Intra− and inter−individ− ual variance of the different components of energy expenditure is variable (cv intra of 5 % for REE and up to 22.7 % for movement, cv inter of 4.5 % for measurements of 24h−EE within a respiration chamber up to 69.2 for AEE under real life conditions). Suitable methods should be selected based on feasibility, the variable of interest, methodological know how and equipment as well as the precision and accuracy of the method. There are new pre− diction formulas for energy expenditure in humans.
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