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Journal articles on the topic 'Oxidative Aging'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 February 2022

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1

Neki, N. S. "Oxidative Stress and Aging." Bangladesh Journal of Medical Science 14, no. 3 (June 20, 2015): 221–27. http://dx.doi.org/10.3329/bjms.v14i3.23468.

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Ageing is an inevitable life process characterized by a gradual functional decline of all organ systems occurring at the cellular, tissue, organ and whole body levels further leading to the development of diseases and finally death. Although aging is a normal physiological process, it can be accelerated during oxidative stress or during chronic inflammatory conditions. An appropriate theory must explain four main characteristics of ageing: it is endogenous, progressive, irreversible and deleterious for the individual. Oxidative stress is caused by imbalance between oxidants and antioxidants. Reactive Oxygen Species (ROS) not only cause cell damage, but are also involved in intracellular signaling. ROS include superoxide (O2-), hydrogen peroxide (H2O2), hydroxyl radical (OH-) and peroxynitrite. Various enzyme systems produce ROS including the mitochondrial electron transport chain, cytochrome P450, lipoxygenase, cyclooxygenase, the NADPH oxidase complex, xanthine oxidase and peroxisomes. More research is needed to explain the exact mechanisms related to ageing and oxidative stress.Bangladesh Journal of Medical Science Vol.14(3) 2015 p.221-227

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2

Szarka, András, Gábor Bánhegyi, and Balázs Sümegi. "Mitochondria, oxidative stress and aging." Orvosi Hetilap 155, no. 12 (March 2014): 447–52. http://dx.doi.org/10.1556/oh.2014.29852.

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The free radical theory of aging was defined in the 1950s. On the base of this theory, the reactive oxygen species formed in the metabolic pathways can play pivotal role in ageing. The theory was modified by defining the mitochondrial respiration as the major cellular source of reactive oxygen species and got the new name mitochondrial theory of aging. Later on the existence of a “vicious cycle” was proposed, in which the reactive oxygen species formed in the mitochondrial respiration impair the mitochondrial DNA and its functions. The formation of reactive oxygen species are elevated due to mitochondrial dysfunction. The formation of mitochondrial DNA mutations can be accelerated by this “vicious cycle”, which can lead to accelerated aging. The exonuclease activity of DNA polymerase γ, the polymerase responsible for the replication of mitochondrial DNA was impaired in mtDNA mutator mouse recently. The rate of somatic mutations in mitochondrial DNA was elevated and an aging phenotype could have been observed in these mice. Surprisingly, no oxidative impairment neither elevated reactive oxygen species formation could have been observed in the mtDNA mutator mice, which may question the existence of the “vicious cycle”. Orv. Hetil., 2014, 155(12), 447–452.

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3

Rad, Farhad Yousefi, Michael D. Elwardany, Cassie Castorena, and Y. Richard Kim. "Evaluation of Chemical and Rheological Aging Indices to Track Oxidative Aging of Asphalt Mixtures." Transportation Research Record: Journal of the Transportation Research Board 2672, no. 28 (June 29, 2018): 349–58. http://dx.doi.org/10.1177/0361198118784138.

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Oxidative age hardening in asphalt binder leads to embrittlement. Embrittled asphalt is prone to fatigue and thermal cracking. Therefore, the ability to predict asphalt binder oxidative age hardening within a pavement throughout its service life could inform improved pavement material selection, design, and maintenance practices. Studying the evolution of oxidative aging requires the use of key properties to track oxidation levels, termed aging index properties (AIPs) here. The objective of this study is to identify suitable rheological and chemical AIPs to track oxidation levels in asphalt materials. A wide range of laboratory and field aged materials were evaluated in this study. A range of chemical AIPs determined by Fourier transform infrared spectroscopy (FTIR) absorbance peaks and areas were evaluated based on their correlation with laboratory aging duration. Rheological AIPs were evaluated based on the strength of their relationship to the chemical changes induced by oxidation. The rheological AIPs evaluated included the dynamic shear modulus, zero shear viscosity, Glover-Rowe parameter, and crossover modulus. The chemical AIP evaluation that most strongly correlated with laboratory aging duration is the carbonyl plus the sulfoxide absorbance peaks. The results indicate that both the dynamic shear modulus and Glover-Rowe parameter constitute rheological AIPs that relate directly to the chemical changes induced by oxidation.

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4

Haenold, Ronny, D. Mokhtar Wassef, Stefan H. Heinemann, and Toshinori Hoshi. "Oxidative damage, aging and anti-aging strategies." AGE 27, no. 3 (September 2005): 183–99. http://dx.doi.org/10.1007/s11357-005-2915-0.

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5

NIKI, Etsuo. "Oxidative Stress and Aging." Internal Medicine 39, no. 4 (2000): 324–26. http://dx.doi.org/10.2169/internalmedicine.39.324.

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6

Rattan, Suresh I. S. "Oxidative stress and aging." FEBS Letters 381, no. 3 (March 4, 1996): 262. http://dx.doi.org/10.1016/s0014-5793(96)90651-1.

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7

Junqueira, Virginia B. C., Silvia B. M. Barros, Sandra S. Chan, Luciano Rodrigues, Leandro Giavarotti, Ronaldo L. Abud, and Guilherme P. Deucher. "Aging and oxidative stress." Molecular Aspects of Medicine 25, no. 1-2 (February 2004): 5–16. http://dx.doi.org/10.1016/j.mam.2004.02.003.

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8

Abdollahi, Mohammad, Majid Y. Moridani, Okezie I. Aruoma, and Sara Mostafalou. "Oxidative Stress in Aging." Oxidative Medicine and Cellular Longevity 2014 (2014): 1–2. http://dx.doi.org/10.1155/2014/876834.

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9

Chen, Danica. "OXIDATIVE STRESS AND AGING." Free Radical Biology and Medicine 53 (November 2012): S3. http://dx.doi.org/10.1016/j.freeradbiomed.2012.10.006.

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10

Lesnefsky, Edward J., and Charles L. Hoppel. "Oxidative phosphorylation and aging." Ageing Research Reviews 5, no. 4 (November 2006): 402–33. http://dx.doi.org/10.1016/j.arr.2006.04.001.

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11

Warner, Huber R. "Oxidative stress and aging." Experimental Gerontology 31, no. 3 (May 1996): 436–38. http://dx.doi.org/10.1016/0531-5565(95)02036-5.

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12

Зенков, Н. К., П. М. Кожин, А. В. Чечушков, Н. В. Кандалинцева, Г. Г. Мартинович, and Е. Б. Меньщикова. "OXIDATIVE STRESS IN AGING." Успехи геронтологии, no. 1 (April 12, 2020): 10–22. http://dx.doi.org/10.34922/ae.2020.33.1.001.

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Выдвинутая более 50 лет назад Д. Харманом свободнорадикальная теория старения остается популярной и сегодня. В обзоре проведен анализ возрастных изменений основных эндогенных механизмов продукции активированных кислородных метаболитов (АКМ) и механизмов антиоксидантной защиты. С возрастом генерация АКМ митохондриями, пероксисомами и NAD(P) H -оксидазами усиливается, в то время как транскрипционная активность важной системы поддержания редокс-баланса Keap 1/ Nrf 2/ ARE уменьшается. У старых животных отмечается также низкая активность аутофагии, удаляющей из клеток поврежденные органеллы и агрегированные структуры. Возрастное смещение редокс-баланса в сторону окислительного стресса может являться причиной развития возраст-ассоциированных нейрогеденеративных, аутоиммунных и воспалительных патологий. The free-radical theory of aging, advanced more than 50 years ago by D. Harman, remains popular today. The review analyzes age-related changes in the main endogenous mechanisms of reactive oxygen species (ROS) production and antioxidant defense mechanisms. With age, ROS generation by mitochondria, peroxisomes, and NAD(P)H oxidases is enhanced, while the transcriptional activity of the important system Keap 1/ Nrf 2/ ARE maintaining redox balance decreases. In old animals, autophagy activity is also low, which removes damaged organelles and aggregated structures from cells. The age-related shift of the redox balance towards oxidative stress can cause the development of age-associated neurodegenerative, autoimmune and inﬂ ammatory pathologies.

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13

Tanakol, Ali, Tuğba Kevser Uzunçakmak, and Zekayi Kutlubay. "Oxidative Stress and Aging." Dermatoz 11, no. 3 (March 16, 2021): 31–35. http://dx.doi.org/10.4274/dermatoz.galenos.2021.68077.

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14

Zhang, Xuemei, and Inge Hoff. "Comparative Study of Thermal-Oxidative Aging and Salt Solution Aging on Bitumen Performance." Materials 14, no. 5 (March 3, 2021): 1174. http://dx.doi.org/10.3390/ma14051174.

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The aging of bitumen is detrimental to the durability and service life of asphalt pavement. Previous studies found that bitumen was suspected to be aged by not only thermal oxidation but also solution immersion. This research aims to compare the effect of thermal-oxidative aging and salt solution aging on bitumen performance. For this purpose, a thin film oven test (TFOT) and pressure aging vessel aging (PAV) were selected as thermal-oxidative aging, and 10% NaCl aging and 10% CaCl2 aging were selected as salt solution aging. The morphology, oxygen content, physical properties, low-temperature properties, and high-temperature properties of bitumen were analysed by employing scanning electron microscopy with an energy dispersive spectrometer (SEM-EDS), physical tests, a bending beam rheometer (BBR), and a dynamic shear rheometer (DSR). Test results show that both thermal-oxidative aging and salt solution aging had similar influencing trends in the oxygen content, physical, low-temperature, and high-temperature properties of bitumen but had different changes in morphology. The aging degrees caused by four kinds of aging methods were obtained based on the summed values of the absolute aging factor of all parameters: PAV > 10% NaCl > TFOT > 10% CaCl2. The conclusions could provide a theoretical basis to establish a standard for the solution aging of bitumen.

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15

Breusing, Nicolle, and Tilman Grune. "Regulation of proteasome-mediated protein degradation during oxidative stress and aging." Biological Chemistry 389, no. 3 (March 1, 2008): 203–9. http://dx.doi.org/10.1515/bc.2008.029.

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Abstract Protein degradation is a physiological process required to maintain cellular functions. There are distinct proteolytic systems for different physiological tasks under changing environmental and pathophysiological conditions. The proteasome is responsible for the removal of oxidatively damaged proteins in the cytosol and nucleus. It has been demonstrated that proteasomal degradation increases due to mild oxidation, whereas at higher oxidant levels proteasomal degradation decreases. Moreover, the proteasome itself is affected by oxidative stress to varying degrees. The ATP-stimulated 26S proteasome is sensitive to oxidative stress, whereas the 20S form seems to be resistant. Non-degradable protein aggregates and cross-linked proteins are able to bind to the proteasome, which makes the degradation of other misfolded and damaged proteins less efficient. Consequently, inhibition of the proteasome has dramatic effects on cellular aging processes and cell viability. It seems likely that during oxidative stress cells are able to keep the nuclear protein pool free of damage, while cytosolic proteins may accumulate. This is because of the high proteasome content in the nucleus, which protects the nucleus from the formation and accumulation of non-degradable proteins. In this review we highlight the regulation of the proteasome during oxidative stress and aging.

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16

Berlett, Barbara S., and Earl R. Stadtman. "Protein Oxidation in Aging, Disease, and Oxidative Stress." Journal of Biological Chemistry 272, no. 33 (August 15, 1997): 20313–16. http://dx.doi.org/10.1074/jbc.272.33.20313.

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17

Moreira, Priscila Lucelia, Paulo Jose Fortes Villas Boas, and Ana Lucia Anjos Ferreira. "Association between oxidative stress and nutritional status in the elderly." Revista da Associação Médica Brasileira 60, no. 1 (February 2014): 75–83. http://dx.doi.org/10.1590/1806-9282.60.01.016.

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Ageing is a dynamic and progressive process that is characterized by the occurrence of morphological, biochemical, functional and psychological changes in the organism. The aim of the present article is to provide updated concepts on oxidative stress, covering its importance in aging, as well as nutritional status and supplementation with antioxidants (substances that prevent or attenuate oxidation of oxidizable substrates, such as lipids, proteins, carbohydrates and deoxyribonucleic acid) in the geriatric population. Evidence suggests that there is an inverse relationship between oxidative stress and nutritional status in elderly individuals. Although an increase in oxidative stress in chronic diseases associated with aging has been proven, such as Parkinson’s disease and Alzheimer’s disease, up to now there has been no consistent clinical evidence proving the efficiency of supplementation with antioxidants against oxidative stress. In this context, supplementation is not recommended. On the other hand, the elderly should be encouraged to eat antioxidant foods, such as fruits and vegetables. Maintaining a normal weight (body mass index between 23 and 28 Kg/m2) should also be stimulated.

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18

Kregel, Kevin C., and Hannah J. Zhang. "An integrated view of oxidative stress in aging: basic mechanisms, functional effects, and pathological considerations." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 292, no. 1 (January 2007): R18—R36. http://dx.doi.org/10.1152/ajpregu.00327.2006.

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Aging is an inherently complex process that is manifested within an organism at genetic, molecular, cellular, organ, and system levels. Although the fundamental mechanisms are still poorly understood, a growing body of evidence points toward reactive oxygen species (ROS) as one of the primary determinants of aging. The “oxidative stress theory” holds that a progressive and irreversible accumulation of oxidative damage caused by ROS impacts on critical aspects of the aging process and contributes to impaired physiological function, increased incidence of disease, and a reduction in life span. While compelling correlative data have been generated to support the oxidative stress theory, a direct cause-and-effect relationship between the accumulation of oxidatively mediated damage and aging has not been strongly established. The goal of this minireview is to broadly describe mechanisms of in vivo ROS generation, examine the potential impact of ROS and oxidative damage on cellular function, and evaluate how these responses change with aging in physiologically relevant situations. In addition, the mounting genetic evidence that links oxidative stress to aging is discussed, as well as the potential challenges and benefits associated with the development of antiaging interventions and therapies.

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19

Zhuang, Tao, Ti Kun Shan, and Li Ling Zhou. "Research on the Thermal Oxidation and Ultraviolet Radiation Aging of Nano-ZnO/NR Composite." Advanced Materials Research 87-88 (December 2009): 462–67. http://dx.doi.org/10.4028/www.scientific.net/amr.87-88.462.

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To study the effection of nano-ZnO on thermal oxidative aging and ultraviolet radiation aging of NR, and the mechanisms of thermal oxidation aging and ultraviolet radiation aging of nano ZnO in NR were explained by TG and stress relaxation and ultraviolet analysis. The results revealed that nano-ZnO can improve the anti-thermal oxidation aging and anti-ultraviolet radiation aging of NR, and the protective effect improves with the increase dose of nano-ZnO.

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20

Huh, Jung-Do, and Raymond E. Robertson. "Modeling of Oxidative Aging Behavior of Asphalts from Short-Term, High-Temperature Data as a Step toward Prediction of Pavement Aging." Transportation Research Record: Journal of the Transportation Research Board 1535, no. 1 (January 1996): 91–97. http://dx.doi.org/10.1177/0361198196153500112.

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The oxidative aging data collected during the Strategic Highway Research Program have been analyzed in terms of kinetics of viscosity change with time and temperature. Changes in viscosity have been used as the measure of the progress of aging. The objective is to model viscosity increases accurately enough to be able to predict aging (in terms of viscosity changes) at pavement temperatures from short-term test data acquired at high temperature. This involved constituting a mathematical model, based on oxidative reactions, and a nonlinear regression of the data to test predictability of the proposed model. Clearly, there is a point beyond which viscosity change becomes independent of time, but no data were collected to that extent. Separately, it has been shown that oxidation of aliphatic sulfide to sulfoxide and oxidation of benzylic carbon to carbonyl are the principal chemical reactions that contribute to an increase in viscosity. The data fit the proposed equation sufficiently well to allow calculation of rate constants of viscosity increases for both reactions, and, hence, allow development of an Arrhenius temperature relationship. Finally, it is hoped that the proposed equation will provide reasonable estimates of rates of oxidative aging of asphalts at pavement temperatures from short-term, high-temperature oxidative aging data measured in a laboratory.

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21

Petersen, J. Claine, and P. Michael Harnsberger. "Asphalt Aging: Dual Oxidation Mechanism and Its Interrelationships with Asphalt Composition and Oxidative Age Hardening." Transportation Research Record: Journal of the Transportation Research Board 1638, no. 1 (January 1998): 47–55. http://dx.doi.org/10.3141/1638-06.

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The kinetic data and chemistry of asphalt oxidative age hardening suggested a sequential, dual mechanism for asphalt oxidation. The dual mechanism rationalizes conflicts between earlier mechanistic investigations and explains the hyperbolic-like, time-versus-property plots characteristic of asphalt oxidative aging. The oxidation kinetics provide further confirmation of the asphalt microstructural model. It is proposed that the rapid initial oxidation rate of asphalt results from reaction of oxygen with limited amounts of highly reactive hydrocarbons. Final oxidation products of this initial reaction are sulfoxides and, most likely, ring aromatization. During this initial reaction, a slower oxidation reaction of asphalt benzylic carbons is initiated; final products are ketones and sulfoxides. The ratio of ketones to sulfoxides formed and the rate of age hardening were found to be dependent on temperature and oxygen pressure. Low-temperature oxidative aging, as occurs in pavements, was found significantly more sensitive to variations in temperature and asphalt composition than 100°C pressure vessel aging.

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22

Doria, Enrico, Daniela Buonocore, Angela Focarelli, and Fulvio Marzatico. "Relationship between Human Aging Muscle and Oxidative System Pathway." Oxidative Medicine and Cellular Longevity 2012 (2012): 1–13. http://dx.doi.org/10.1155/2012/830257.

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Ageing is a complex process that in muscle is usually associated with a decrease in mass, strength, and velocity of contraction. One of the most striking effects of ageing on muscle is known as sarcopenia. This inevitable biological process is characterized by a general decline in the physiological and biochemical functions of the major systems. At the cellular level, aging is caused by a progressive decline in mitochondrial function that results in the accumulation of reactive oxygen species (ROS) generated by the addition of a single electron to the oxygen molecule. The aging process is characterized by an imbalance between an increase in the production of reactive oxygen species in the organism and the antioxidant defences as a whole. The goal of this review is to examine the results of existing studies on oxidative stress in aging human skeletal muscles, taking into account different physiological factors (sex, fibre composition, muscle type, and function).

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23

Barcelos, Isabella Peixoto de, and Richard H. Haas. "CoQ10 and Aging." Biology 8, no. 2 (May 11, 2019): 28. http://dx.doi.org/10.3390/biology8020028.

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The aging process includes impairment in mitochondrial function, a reduction in anti-oxidant activity, and an increase in oxidative stress, marked by an increase in reactive oxygen species (ROS) production. Oxidative damage to macromolecules including DNA and electron transport proteins likely increases ROS production resulting in further damage. This oxidative theory of cell aging is supported by the fact that diseases associated with the aging process are marked by increased oxidative stress. Coenzyme Q10 (CoQ10) levels fall with aging in the human but this is not seen in all species or all tissues. It is unknown whether lower CoQ10 levels have a part to play in aging and disease or whether it is an inconsequential cellular response to aging. Despite the current lay public interest in supplementing with CoQ10, there is currently not enough evidence to recommend CoQ10 supplementation as an anti-aging anti-oxidant therapy.

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24

Chen, Ge, and Jia Lu Li. "Accelerated Test Design of Thermal-Oxidative Aging of Nylon 66 Airbag Material." Advanced Materials Research 332-334 (September 2011): 1202–5. http://dx.doi.org/10.4028/www.scientific.net/amr.332-334.1202.

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Accelerated thermal-oxidative aging tests on Nylon 66 automotive airbag material are designed and performed in this paper. After the environmental profile of airbag was analyzed, Nylon 66 airbag yarns were reasonably selected as the test samples, and its tensile strength was chosen as the significant character of their aging stability. By heat aging、humidity aging、cycle ageing and comprehensive process aging experiments, 350dtex Nylon 66 filament were sampled and the tensile strength loss of samples was measured, to determine the mechanisms and factors that influence aging stability of the Nylon 66 airbag materials. The experiment results show that Nylon 66 has excellent aging stability, and that water molecules can accelerate its degradation. The experiment data can be used to predict the airbag lifetime in a benign store environment, and as references in selecting airbag materials.

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25

Pandey, Kanti Bhooshan, Mohd Murtaza Mehdi, Pawan Kumar Maurya, and Syed Ibrahim Rizvi. "Plasma Protein Oxidation and Its Correlation with Antioxidant Potential During Human Aging." Disease Markers 29, no. 1 (2010): 31–36. http://dx.doi.org/10.1155/2010/964630.

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Previous studies have indicated that the main molecular characteristic of aging is the progressive accumulation of oxidative damages in cellular macromolecules. Proteins are one of the main molecular targets of age-related oxidative stress, which have been observed during aging process in cellular systems. Reactive oxygen species (ROS) can lead to oxidation of amino acid side chains, formation of protein-protein cross-linkages, and oxidation of the peptide backbones. In the present study, we report the age-dependent oxidative alterations in biomarkers of plasma protein oxidation: protein carbonyls (PCO), advanced oxidation protein products (AOPPs) and plasma total thiol groups (T-SH) in the Indian population and also correlate these parameters with total plasma antioxidant potential. We show an age dependent decrease in T-SH levels and increase in PCO and AOPPs level. The alterations in the levels of these parameters correlated significantly with the total antioxidant capacity of the plasma. The levels of oxidized proteins in plasma provide an excellent biomarker of oxidative stress due to the relative long half-life of such oxidized proteins.

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26

Golbidi, Saeid, and Ismail Laher. "Exercise and the Aging Endothelium." Journal of Diabetes Research 2013 (2013): 1–12. http://dx.doi.org/10.1155/2013/789607.

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The endothelium plays a critical role in the maintenance of cardiovascular health by producing nitric oxide and other vasoactive materials. Aging is associated with a gradual decline in this functional aspect of endothelial regulation of cardiovascular homeostasis. Indeed, age is an independent risk factor for cardiovascular diseases and is in part an important factor in the increased exponential mortality rates from vascular disease such as myocardial infarction and stroke that occurs in the ageing population. There are a number of mechanisms suggested to explain age-related endothelial dysfunction. However, recent scientific studies have advanced the notion of oxidative stress and inflammation as the two major risk factors underlying aging and age-related diseases. Regular physical activity, known to have a favorable effect on cardiovascular health, can also improve the function of the ageing endothelium by modulating oxidative stress and inflammatory processes, as we discuss in this paper.

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27

Ahsanuddin, Sayeeda, Minh Lam, and Elma D. Baron. "Skin aging and oxidative stress." AIMS Molecular Science 3, no. 2 (2016): 187–95. http://dx.doi.org/10.3934/molsci.2016.2.187.

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28

Korovila, Ioanna, Martín Hugo, José Pedro Castro, Daniela Weber, Annika Höhn, Tilman Grune, and Tobias Jung. "Proteostasis, oxidative stress and aging." Redox Biology 13 (October 2017): 550–67. http://dx.doi.org/10.1016/j.redox.2017.07.008.

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29

Sastre, Juan, Federico V. Pallardó, José García de la Asunción, and José Viña. "Mitochondria, oxidative stress and aging." Free Radical Research 32, no. 3 (January 2000): 189–98. http://dx.doi.org/10.1080/10715760000300201.

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30

Liu, Dongping, and Yang Xu. "p53, Oxidative Stress, and Aging." Antioxidants & Redox Signaling 15, no. 6 (September 15, 2011): 1669–78. http://dx.doi.org/10.1089/ars.2010.3644.

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31

Yu, Byung Pal, and Hae Young Chung. "Oxidative stress and vascular aging." Diabetes Research and Clinical Practice 54 (December 2001): S73—S80. http://dx.doi.org/10.1016/s0168-8227(01)00338-2.

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32

Liao, Chen-Yu, and Brian K. Kennedy. "SIRT6, oxidative stress, and aging." Cell Research 26, no. 2 (January 19, 2016): 143–44. http://dx.doi.org/10.1038/cr.2016.8.

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33

Liguori, Ilaria, Gennaro Russo, Francesco Curcio, Giulia Bulli, Luisa Aran, David Della-Morte, Gaetano Gargiulo, et al. "Oxidative stress, aging, and diseases." Clinical Interventions in Aging Volume 13 (April 2018): 757–72. http://dx.doi.org/10.2147/cia.s158513.

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34

Shaw, Peter X., Geoff Werstuck, and Yan Chen. "Oxidative Stress and Aging Diseases." Oxidative Medicine and Cellular Longevity 2014 (2014): 1–2. http://dx.doi.org/10.1155/2014/569146.

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35

Gamarra, A., and E. A. Ossa. "Thermo-oxidative aging of bitumen." International Journal of Pavement Engineering 19, no. 7 (June 30, 2016): 641–50. http://dx.doi.org/10.1080/10298436.2016.1199876.

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36

LeBel, Carl P., and Stephen C. Bondy. "Oxidative damage and cerebral aging." Progress in Neurobiology 38, no. 6 (June 1992): 601–9. http://dx.doi.org/10.1016/0301-0082(92)90043-e.

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37

Sastre, Juan, Federico V. Pallardó, and Jose Viña. "Glutathione, oxidative stress and aging." AGE 19, no. 4 (October 1996): 129–39. http://dx.doi.org/10.1007/bf02434082.

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38

Agarwal, Sanjiv, and R. S. Sohal. "Aging and protein oxidative damage." Mechanisms of Ageing and Development 75, no. 1 (July 1994): 11–19. http://dx.doi.org/10.1016/0047-6374(94)90024-8.

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39

Muller, Florian L., Michael S. Lustgarten, Youngmok Jang, Arlan Richardson, and Holly Van Remmen. "Trends in oxidative aging theories." Free Radical Biology and Medicine 43, no. 4 (August 15, 2007): 477–503. http://dx.doi.org/10.1016/j.freeradbiomed.2007.03.034.

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40

Ames, Bruce N. "Oxidative DNA damage and aging." Free Radical Biology and Medicine 9 (January 1990): 45. http://dx.doi.org/10.1016/0891-5849(90)90326-e.

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41

Starke-Reed, Pamela E., and Cynthia N. Oliver. "Protein oxidation and proteolysis during aging and oxidative stress." Archives of Biochemistry and Biophysics 275, no. 2 (December 1989): 559–67. http://dx.doi.org/10.1016/0003-9861(89)90402-5.

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42

Pochiraju, K. V., and G. P. Tandon. "Modeling Thermo-Oxidative Layer Growth in High-Temperature Resins." Journal of Engineering Materials and Technology 128, no. 1 (August 1, 2005): 107–16. http://dx.doi.org/10.1115/1.2128427.

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This paper describes modeling of degradation behavior of high-temperature polymers under thermo-oxidative aging conditions. Thermo-oxidative aging is simulated with a diffusion-reaction model in which temperature, oxygen concentration, and weight-loss effects are considered. A parametric reaction model based on a mechanistic view of the reaction is used for simulating reaction-rate dependence on the oxygen availability in the polymer. Macroscopic weight-loss measurements are used to determine the reaction and polymer consumption parameters. The diffusion-reaction partial differential equation system is solved using Runge-Kutta methods. Simulations illustrating oxidative layer growth in a high-temperature PMR-15 polyimide resin system under isothermal conditions are presented and correlated with experimental observations of oxidation layer growth. Finally, parametric studies are conducted to examine the sensitivity of material parameters in predicting oxidation development.

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Chen, Feng, Yingxia Liu, Nai-Kei Wong, Jia Xiao, and Kwok-Fai So. "Oxidative Stress in Stem Cell Aging." Cell Transplantation 26, no. 9 (September 2017): 1483–95. http://dx.doi.org/10.1177/0963689717735407.

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Stem cell aging is a process in which stem cells progressively lose their ability to self-renew or differentiate, succumb to senescence or apoptosis, and eventually become functionally depleted. Unresolved oxidative stress and concomitant oxidative damages of cellular macromolecules including nucleic acids, proteins, lipids, and carbohydrates have been recognized to contribute to stem cell aging. Excessive production of reactive oxygen species and insufficient cellular antioxidant reserves compromise cell repair and metabolic homeostasis, which serves as a mechanistic switch for a variety of aging-related pathways. Understanding the molecular trigger, regulation, and outcomes of those signaling networks is critical for developing novel therapies for aging-related diseases by targeting stem cell aging. Here we explore the key features of stem cell aging biology, with an emphasis on the roles of oxidative stress in the aging process at the molecular level. As a concept of cytoprotection of stem cells in transplantation, we also discuss how systematic enhancement of endogenous antioxidant capacity before or during graft into tissues can potentially raise the efficacy of clinical therapy. Finally, future directions for elucidating the control of oxidative stress and developing preventive/curative strategies against stem cell aging are discussed.

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Sun, Zhuo Jun, Jian Gao, Hui Liu, Shu Zhen Pan, Shu Li Zhang, Lun Hua Yang, Xiao Yun Song, and Jian Guo Gao. "Migration Characteristics and Degradation Kinetics of Bisphenol A." Materials Science Forum 850 (March 2016): 128–36. http://dx.doi.org/10.4028/www.scientific.net/msf.850.128.

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This paper study the migration characteristics and degradation kinetics of bisphenol A using TGA - gas chromatography - mass spectrometry and found that bisphenol A polycarbonate in the thermal oxidative aging conditions of 130 °C de-gradated to bisphenol A. At the range of 0 h to 120 h, the bisphenol A content of environmental hormones increased with time. When it reached 120 h, bisphenol A environmental hormone content decreased slightly with aging time. The content of bisphenol A reached 495mg/kg when the thermal oxidative aging time was 168 h, which was decreased compared to the content of 442mg/kg at 120 h. Polycarbonate thermal decomposition kinetics study showed that the thermal decomposition of polycarbonate can be divided into three phases. The first thermal decomposition occurred at the range of 415° C to 425 ° C, the polycarbonate end groups fracture of the second stage at 493.6°C , the main fracture of the main chain rearrangement and crosslinking, and the third stage at 598.7°C, the degradation of the chain continues to decompose and the decomposition of the crosslinked carbon precursor; thermal oxidation aging of polycarbonate decreased the heat stability and promote the thermal decomposition of polycarbonate. Comparing the oxidation induction period, thermal weight loss rate and activation energy of polycarbonate before and after thermal oxidative aging, it c found that the thermal stability of the hot oxygen aging of polycarbonate is reduced.

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Cui, Hang, Yahui Kong, and Hong Zhang. "Oxidative Stress, Mitochondrial Dysfunction, and Aging." Journal of Signal Transduction 2012 (October 2, 2012): 1–13. http://dx.doi.org/10.1155/2012/646354.

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Aging is an intricate phenomenon characterized by progressive decline in physiological functions and increase in mortality that is often accompanied by many pathological diseases. Although aging is almost universally conserved among all organisms, the underlying molecular mechanisms of aging remain largely elusive. Many theories of aging have been proposed, including the free-radical and mitochondrial theories of aging. Both theories speculate that cumulative damage to mitochondria and mitochondrial DNA (mtDNA) caused by reactive oxygen species (ROS) is one of the causes of aging. Oxidative damage affects replication and transcription of mtDNA and results in a decline in mitochondrial function which in turn leads to enhanced ROS production and further damage to mtDNA. In this paper, we will present the current understanding of the interplay between ROS and mitochondria and will discuss their potential impact on aging and age-related diseases.

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Olinski, Ryszard, Agnieszka Siomek, Rafal Rozalski, Daniel Gackowski, Marek Foksinski, Jolanta Guz, Tomasz Dziaman, Anna Szpila, and Barbara Tudek. "Oxidative damage to DNA and antioxidant status in aging and age-related diseases." Acta Biochimica Polonica 54, no. 1 (January 9, 2007): 11–26. http://dx.doi.org/10.18388/abp.2007_3265.

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Aging is a complex process involving morphologic and biochemical changes in single cells and in the whole organism. One of the most popular explanations of how aging occurs at the molecular level is the oxidative stress hypothesis. Oxidative stress leads in many cases to an age-dependent increase in the cellular level of oxidatively modified macromolecules including DNA, and it is this increase which has been linked to various pathological conditions, such as aging, carcinogenesis, neurodegenerative and cardiovascular diseases. It is, however, possible that a number of short-comings associated with gaps in our knowledge may be responsible for the failure to produce definite results when applied to understanding the role of DNA damage in aging and age-related diseases.

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Salmon, Adam B., Arlan Richardson, and Viviana I. Pérez. "Update on the oxidative stress theory of aging: Does oxidative stress play a role in aging or healthy aging?" Free Radical Biology and Medicine 48, no. 5 (March 2010): 642–55. http://dx.doi.org/10.1016/j.freeradbiomed.2009.12.015.

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Friguet, Bertrand. "Protein Repair and Degradation during Aging." Scientific World JOURNAL 2 (2002): 248–54. http://dx.doi.org/10.1100/tsw.2002.98.

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Cellular aging is characterized by a build-up of oxidatively modified proteins. The steady-state level of oxidized proteins depends on the balance between the rate of protein oxidative damage and the rates of protein degradation and repair. Therefore, the accumulation of oxidized protein with age can be due to increased protein damage, decreased oxidized protein degradation and repair, or the combination of both mechanisms. The proteasomal system is the major intracellular proteolytic pathway implicated in the degradation of oxidized protein, and the peptide methionine sulfoxide reductase catalyzes the reduction of methionine sulfoxide (i.e., oxidized methionine) to methionine within proteins. A short summary on protein oxidative damage and oxidized protein degradation is given, and evidence for a decline of proteasome function with age is presented. Arguments for the implication of peptide methionine sulfoxide reductase in the age-related accumulation of oxidized protein are also discussed.

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Oliveira, Monique Cristine de, and João Paulo Ferreira Schoffen. "Oxidative stress action in cellular aging." Brazilian Archives of Biology and Technology 53, no. 6 (December 2010): 1333–42. http://dx.doi.org/10.1590/s1516-89132010000600009.

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Various theories try to explain the biological aging by changing the functions and structure of organic systems and cells. During lifetime, free radicals in the oxidative stress lead to lipid peroxidation of cellular membranes, homeostasis imbalance, chemical residues formation, gene mutations in DNA, dysfunction of certain organelles, and the arise of diseases due to cell death and/or injury. This review describes the action of oxidative stress in the cells aging process, emphasizing the factors such as cellular oxidative damage, its consequences and the main protective measures taken to prevent or delay this process. Tests with antioxidants: vitamins A, E and C, flavonoids, carotenoids and minerals, the practice of caloric restriction and physical exercise, seeking the beneficial effects on human health, increasing longevity, reducing the level of oxidative stress, slowing the cellular senescence and origin of certain diseases, are discussed.

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DAS, Nilanjana, Rodney L. LEVINE, William C. ORR, and Rajindar S. SOHAL. "Selectivity of protein oxidative damage during aging in Drosophila melanogaster." Biochemical Journal 360, no. 1 (November 8, 2001): 209–16. http://dx.doi.org/10.1042/bj3600209.

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The purpose of the present study was to determine whether oxidation of various proteins during the aging process occurs selectively or randomly, and whether the same proteins are damaged in different species. Protein oxidative damage to the proteins, present in the matrix of mitochondria in the flight muscles of Drosophila melanogaster and manifested as carbonyl modifications, was detected immunochemically with anti-dinitrophenyl-group antibodies. Aconitase was found to be the only protein in the mitochondrial matrix that exhibited an age-associated increase in carbonylation. The accrual of oxidative damage was accompanied by an approx. 50% loss in aconitase activity. An increase in ambient temperature, which elevates the rate of metabolism and shortens the life span of flies, caused an elevation in the amount of aconitase carbonylation and an accelerated loss in its activity. Exposure to 100% ambient oxygen showed that aconitase was highly susceptible to undergo oxidative damage and loss of activity under oxidative stress. Administration of fluoroacetate, a competitive inhibitor of aconitase activity, resulted in a dose-dependent decrease in the life span of the flies. Results of the present study demonstrate that protein oxidative damage during aging is a selective phenomenon, and might constitute a mechanism by which oxidative stress causes age-associated losses in specific biochemical functions.

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