scholarly journals Plasma Protein Oxidation and Its Correlation with Antioxidant Potential During Human Aging

2010 ◽  
Vol 29 (1) ◽  
pp. 31-36 ◽  
Author(s):  
Kanti Bhooshan Pandey ◽  
Mohd Murtaza Mehdi ◽  
Pawan Kumar Maurya ◽  
Syed Ibrahim Rizvi
Keyword(s):  
Oxidative Stress ◽  
Plasma Protein ◽  
Protein Oxidation ◽  
Cellular Systems ◽  
Antioxidant Potential ◽  
Protein Carbonyls ◽  
Oxidized Proteins ◽  
Oxidative Damages ◽  
Age Related ◽  
Age Dependent

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.

scholarly journals Plasma Protein Carbonyls as Biomarkers of Oxidative Stress in Chronic Kidney Disease, Dialysis, and Transplantation

2020 ◽  
Vol 2020 ◽  
pp. 1-20 ◽  
Author(s):  
Graziano Colombo ◽  
Francesco Reggiani ◽  
Claudio Angelini ◽  
Silvia Finazzi ◽  
Emanuela Astori ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Peritoneal Dialysis ◽  
Kidney Transplantation ◽  
Renal Replacement Therapy ◽  
Oxidative Damage ◽  
Plasma Protein ◽  
Protein Carbonyls ◽  
Ckd Progression ◽  
Biomarkers Of Oxidative Stress

Accumulating evidence indicates that oxidative stress plays a role in the pathophysiology of chronic kidney disease (CKD) and its progression; during renal replacement therapy, oxidative stress-derived oxidative damage also contributes to the development of CKD systemic complications, such as cardiovascular disease, hypertension, atherosclerosis, inflammation, anaemia, and impaired host defence. The main mechanism underlying these events is the retention of uremic toxins, which act as a substrate for oxidative processes and elicit the activation of inflammatory pathways targeting endothelial and immune cells. Due to the growing worldwide spread of CKD, there is an overwhelming need to find oxidative damage biomarkers that are easy to measure in biological fluids of subjects with CKD and patients undergoing renal replacement therapy (haemodialysis, peritoneal dialysis, and kidney transplantation), in order to overcome limitations of invasive monitoring of CKD progression. Several studies investigated biomarkers of protein oxidative damage in CKD, including plasma protein carbonyls (PCO), the most frequently used biomarker of protein damage. This review provides an up-to-date overview on advances concerning the correlation between plasma protein carbonylation in CKD progression (from stage 1 to stage 5) and the possibility that haemodialysis, peritoneal dialysis, and kidney transplantation improve plasma PCO levels. Despite the fact that the role of plasma PCO in CKD is often underestimated in clinical practice, emerging evidence highlights that plasma PCO can serve as good biomarkers of oxidative stress in CKD and substitutive therapies. Whether plasma PCO levels merely serve as biomarkers of CKD-related oxidative stress or whether they are associated with the pathogenesis of CKD complications deserves further evaluation.

scholarly journals Reduced mitochondrial ROS, enhanced antioxidant defense, and distinct age-related changes in oxidative damage in muscles of long-lived Peromyscus leucopus

2013 ◽  
Vol 304 (5) ◽  
pp. R343-R355 ◽  
Author(s):  
Yun Shi ◽  
Daniel A. Pulliam ◽  
Yuhong Liu ◽  
Ryan T. Hamilton ◽  
Amanda L. Jernigan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Peromyscus Leucopus ◽  
Laboratory Mouse ◽  
Linear Increase ◽  
Young Age ◽  
Protein Carbonyls ◽  
Ros Generation ◽  
Glutathione Peroxidase 1 ◽  
Age Related

Comparing biological processes in closely related species with divergent life spans is a powerful approach to study mechanisms of aging. The oxidative stress hypothesis of aging predicts that longer-lived species would have lower reactive oxygen species (ROS) generation and/or an increased antioxidant capacity, resulting in reduced oxidative damage with age than in shorter-lived species. In this study, we measured ROS generation in the young adult animals of the long-lived white-footed mouse, Peromyscus leucopus (maximal life span potential, MLSP = 8 yr) and the common laboratory mouse, Mus musculus (C57BL/6J strain; MLSP = 3.5 yr). Consistent with the hypothesis, our results show that skeletal muscle mitochondria from adult P. leucopus produce less ROS (superoxide and hydrogen peroxide) compared with M. musculus. Additionally, P. leucopus has an increase in the activity of antioxidant enzymes superoxide dismutase 1, catalase, and glutathione peroxidase 1 at young age. P. leucopus compared with M. musculus display low levels of lipid peroxidation (isoprostanes) throughout life; however, P. leucopus although having elevated protein carbonyls at a young age, the accrual of protein oxidation with age is minimal in contrast to the linear increase in M. musculus. Altogether, the results from young animals are in agreement with the predictions of the oxidative stress hypothesis of aging with the exception of protein carbonyls. Nonetheless, the age-dependent increase in protein carbonyls is more pronounced in short-lived M. musculus, which supports enhanced protein homeostasis in long-lived P. leucopus.

scholarly journals The effect of elderly simulated gastrointestinal in vitro digestion (SGID) on the antioxidant properties of different cheese matrices

2020 ◽  
Vol 79 (OCE2) ◽  
Author(s):  
Aimee M. Plante ◽  
Aoife L. McCarthy ◽  
Fiona O'Halloran
Keyword(s):  
Oxidative Stress ◽  
Radical Scavenging ◽  
Antioxidant Potential ◽  
Total Phenolic ◽  
Physiological Changes ◽  
Negative Effects ◽  
Antioxidant Power ◽  
Age Related ◽  
Cheese Products

AbstractThe world's population is getting older. By 2050 it is projected that 22% of the global population will be over 60 years of age. Aging is characterized by a decline in physiological functions and an increase in malnutrition and associated disease. Oxidative stress is associated with several age-related conditions, including cardiovascular disease, obesity, neurodegenerative disease and cancer. The negative effects of reactive oxygen species (ROS) are neutralized by antioxidants, which can be endogenously synthesised or consumed through the diet. Cheese is a nutritious dairy food and previous research has highlighted the antioxidant potential of some cheese types. Physiological changes associated with age can impact digestion processes, thus the ability to efficiently release bioactive compounds, including antioxidants, may be impaired with age. Cheese products varying by milk source, texture and fat content were subjected to simulated gastrointestinal in vitro digestion (SGID) using a modified model to account for physiological changes associated with aging. The antioxidant potential of undigested and digested cheese (n = 11) was determined in vitro using DPPH radical scavenging, ferric reducing antioxidant power (FRAP) and total phenolic content (TPC) assays. Cellular antioxidant potential was also investigated using the reduced glutathione assay (GSH) in the human macrophage cell line (U937). Experiments were carried out in triplicate. Statistical analysis by T-test demonstrated that digestion significantly increased (P < 0.05) FRAP and TPC of all cheese products analysed. Of the eleven cheese products investigated, goats’ cheese displayed a significant increase (P < 0.05) in radical scavenging properties (89.8% inhibition). Low fat white cheddar had significantly higher (P < 0.05) GSH levels compared to full fat white cheddar (0.16 ± 0.01, 0.11 ± 0.01 μmol GSH/mg protein, respectively). Findings from this study suggest that despite physiological changes associated with age, cheese digestates retain, and in some cases, possess higher antioxidant potential than undigested samples. Cheese demonstrates potential as a functional food for the elderly by neutralizing the negative effects associated with age-related oxidative stress.

scholarly journals Depletion of the Third Complement Component Ameliorates Age-Dependent Oxidative Stress and Positively Modulates Autophagic Activity in Aged Retinas in a Mouse Model

2017 ◽  
Vol 2017 ◽  
pp. 1-17 ◽  
Author(s):  
Dorota Rogińska ◽  
Miłosz P. Kawa ◽  
Ewa Pius-Sadowska ◽  
Renata Lejkowska ◽  
Karolina Łuczkowska ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Global Gene Expression ◽  
Complement Component ◽  
Oxidative Stress Marker ◽  
Age Related ◽  
Age Dependent ◽  
Autophagic Activity

The aim of the study was to investigate the influence of complement component C3 global depletion on the biological structure and function of the aged retina. In vivo morphology (OCT), electrophysiological function (ERG), and the expression of selected oxidative stress-, apoptosis-, and autophagy-related proteins were assessed in retinas of 12-month-old C3-deficient and WT mice. Moreover, global gene expression in retinas was analyzed by RNA arrays. We found that the absence of active C3 was associated with (1) alleviation of the age-dependent decrease in retinal thickness and gradual deterioration of retinal bioelectrical function, (2) significantly higher levels of antioxidant enzymes (catalase and glutathione reductase) and the antiapoptotic survivin and Mcl-1/Bak dimer, (3) lower expression of the cellular oxidative stress marker—4HNE—and decreased activity of proapoptotic caspase-3, (4) ameliorated retinal autophagic activity with localization of ubiquitinated protein conjugates commonly along the retinal pigment epithelium (RPE) layer, and (5) significantly increased expression of several gene sets associated with maintenance of the physiological functions of the neural retina. Our findings shed light on mechanisms of age-related retinal alterations by identifying C3 as a potential therapeutic target for retinal aging.

Plasma Protein Oxidation and Triglyceride Levels in Sickle Cell Anemia.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 2578-2578
Author(s):  
Yesim Oztas ◽  
Selma Unal ◽  
Nuriman Ozgunes
Keyword(s):  
Oxidative Stress ◽  
Sickle Cell ◽  
Plasma Protein ◽  
Sickle Cell Anemia ◽  
Protein Oxidation ◽  
Conflicts Of Interest ◽  
Protein Carbonyl ◽  
Healthy Children ◽  
Healthy Controls ◽  
Lipid Balance

Abstract Abstract 2578 Poster Board II-555 Introduction: A mutant and unstable hemoglobin is characteristic in sickle cell anemia (SCA) with an increased formation of methemoglobin, hemichrome and haemin. Increased oxidative stress and altered lipid balance in the plasmas of SCA patients have been documented previously. Lower total plasma cholesterol (TC) and higher-than-avarage triglyceride (TG) levels have also been reported in SCA patients compared to healthy controls. Plasma phospholipids (PL) were normal or increased according to various studies. However, to our knowledge only a few reports documented the plasma protein oxidation in SCA patients. In this study protein oxidation, lipid levels, bilurubin levels and their probable correlation were investigated in the plasmas of SCA patients, carriers and healthy controls. Patient and Methods: 15 SCA patients, 10 carriers and 10 healthy controls were included in the study. The patients had not been transfused and hospitalized and had no crisis for the last three months. The oxidation status of plasma and its proteins were detirmined by total sulfhydryl (T-SH) and protein carbonly levels respectively. TC, TG and bilurubin levels were detirmined in the plasma and PL levels were detirmined in the lipid extract from plasma. Results: SCA patients had lower T-SH levels compared to controls (p=0.003) and higher protein carbonyl levels compared to carriers (p=0.001) and healthy children (p=0.032). T-SH values were 417.41±77.90 μM, 457.46±106.26 μM, 522.59±77.18 μM and protein carbonyl levels were 0.93±0.15 nmol/mg protein, 0.74±0.08 nmol/mg protein , 0.82±0.05 nmol/mg protein for patients, carriers and controls respectively. Significantly lower mean TC levels than controls (p<0.0001) and higher TG levels than carriers (p=0.001) were observed in SCA patients. TC levels were 116.67±23.60, 127.53±22.40, 151.62±16.53 and TG levels were 89.31±23.50 mg/dl, 60.94±9.18 mg/dl, 82.96±21.06 mg/dl for patients, carriers and controls respectively. Phospholipid levels were not different between the groups. TG levels were positively correlated to protein carbonyl levels (p=0.002) and to bilirubin levels (p=0.033). Bilurubin levels and protein carbonyl levels are also positively correlated (p<0,0001). Conclusions: Alteration of lipid balance besides protein oxidation and hemolysis were observed in the plasmas of SCA patients compared to the carriers and healthy group. The positive correlation between total bilurubin, TG and carbonyl levels indicates that oxidative stress may affect the SCA plasma extensively, ie. lipids, proteins and erythrocytes are all affected. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Quantitative proteomic analysis reveals novel mitochondrial targets of estrogen deficiency in the aged female rat heart

2012 ◽  
Vol 44 (20) ◽  
pp. 957-969 ◽  
Author(s):  
T. S. Lancaster ◽  
S. J. Jefferson ◽  
J. Craig Hunter ◽  
Veronica Lopez ◽  
J. E. Van Eyk ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Adenine Nucleotide ◽  
Monoamine Oxidase A ◽  
Coronary Artery Ligation ◽  
Female Rat ◽  
Female Population ◽  
Ovx Rats ◽  
Age Related ◽  
Age Dependent ◽  
Mao A

The incidence of myocardial infarction rises sharply at menopause, implicating a potential role for estrogen (E2) loss in age-related increases in ischemic injury. We aimed to identify quantitative changes to the cardiac mitochondrial proteome of aging females, based on the hypothesis that E2 deficiency exacerbates age-dependent disruptions in mitochondrial proteins. Mitochondria isolated from left ventricles of adult (6 mo) and aged (24 mo) F344 ovary-intact or ovariectomized (OVX) rats were labeled with 8plex isobaric tags for relative and absolute quantification (iTRAQ; n = 5–6/group). Groups studied were adult, adult OVX, aged, and aged OVX. In vivo coronary artery ligation and in vitro mitochondrial respiration studies were also performed in a subset of rats. We identified 965 proteins across groups and significant directional changes in 67 proteins of aged and/or aged OVX; 32 proteins were unique to aged OVX. Notably, only six proteins were similarly altered in adult OVX (voltage-dependent ion channel 1, adenine nucleotide translocator 1, cytochrome c oxidase subunits VIIc and VIc, catalase, and myosin binding protein C). Proteins affected by aging were primarily related to cellular metabolism, oxidative stress, and cell death. The largest change occurred in monoamine oxidase-A (MAO-A), a source of oxidative stress. While acute MAO-A inhibition induced mild uncoupling in aged mitochondria, reductions in infarct size were not observed. Age-dependent alterations in mitochondrial signaling indicate a highly selective myocardial response to E2 deficiency. The combined proteomic and functional approaches described here offer possibility of new protein targets for experimentation and therapeutic intervention in the aged female population.

scholarly journals Potential Implications of Rimonabant on Age-Related Oxidative Stress and Inflammation

Antioxidants ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 162
Author(s):  
Renáta Szabó ◽  
Zsuzsanna Szabó ◽  
Denise Börzsei ◽  
Alexandra Hoffmann ◽  
Zelma Nadin Lesi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Successful Aging ◽  
Defense Mechanisms ◽  
Endocannabinoid System ◽  
Cb1 Receptor ◽  
Necrosis Factor Alpha ◽  
Inflammatory Parameters ◽  
Oxidative Damages ◽  
Age Related ◽  
Tnf Α

Over the last decades, growing interest has turned to preventive and therapeutic approaches for achieving successful aging. Oxidative stress and inflammation are fundamental features of cardiovascular diseases; therefore, potential targets of them can improve cardiac outcomes. Our study aimed to examine the involvement of the endocannabinoid system, especially the CB1 receptor blockade, on inflammatory and oxidant/antioxidant processes. Twenty-month-old female and male Wistar rats were divided into rimonabant-treated and aging control (untreated) groups. Rimonabant, a selective CB1 receptor antagonist, was administered at the dose of 1 mg/kg/day intraperitoneally for 2 weeks. Cardiac amounts of ROS, the antioxidant glutathione and superoxide dismutase (SOD), and the activity and concentration of the heme oxygenase (HO) enzyme were detected. Among inflammatory parameters, nuclear factor-kappa B (NF-κB), tumor necrosis factor-alpha (TNF-α), and myeloperoxidase (MPO) enzyme activity were measured. Two weeks of low dose rimonabant treatment significantly reduced the cardiac ROS via boosting of the antioxidant defense mechanisms as regards the HO system, and the SOD and glutathione content. Consistently, the age-related inflammatory response was alleviated. Rimonabant-treated animals showed significantly decreased NF-κB, TNF-α, and MPO levels. Our findings prove the beneficial involvement of CB1 receptor blocker rimonabant on inflammatory and oxidative damages to the aging heart.

Proteolytic 'defences' and the accumulation of oxidized polypeptides in cataractogenesis and atherogenesis

2003 ◽  
Vol 70 ◽  
pp. 135-146 ◽  
Author(s):  
Roger T. Dean ◽  
Rachael Dunlop ◽  
Peter Hume ◽  
Ken J. Rodgers
Keyword(s):  
Protein Oxidation ◽  
Oxidative Burst ◽  
Connective Tissues ◽  
Oxidized Proteins ◽  
Accelerated Degradation ◽  
Experimental Systems ◽  
Age Related ◽  
Low Levels ◽  
And Control ◽  
Neutrophil Oxidative Burst

Over the last few years, it has been clearly established that normal plasma contains low levels of oxidized polypeptides, and that these accumulate in tissues during several age-related pathologies. In contrast, normal mammalian aging, contrary to conventional dogma, is not clearly associated with enhanced levels of oxidized proteins, except in extracellular connective tissues, whose proteins can, for example, be oxidized by the neutrophil oxidative burst. Since mildly oxidized proteins are susceptible to accelerated degradation in most experimental systems, the question arises as to how the accumulation of oxidized proteins can take place. Such accumulation requires an excess of production (or deposition) over removal, which might reflect alterations in capacity or rate of production or removal. This chapter discusses our presently limited knowledge of rates and control of proteolysis of oxidized proteins in two pathologies, cataractogenesis and atherogenesis. It commences with a brief summary of current understanding of the mechanisms of protein oxidation, and of the observed accumulation of oxidized proteins in several pathologies.

scholarly journals Nucleic acid oxidation is associated with biomarkers of neurodegeneration in CSF in people with HIV

2020 ◽  
Vol 7 (6) ◽  
pp. e902
Author(s):  
Ronald J. Ellis ◽  
David J. Moore ◽  
Erin E. Sundermann ◽  
Robert K. Heaton ◽  
Sanjay Mehta ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nucleic Acid ◽  
Antiretroviral Drugs ◽  
Protein Carbonyls ◽  
Acid Oxidation ◽  
Csf Biomarkers ◽  
Cross Sectional ◽  
Suspension Array ◽  
Total Tau ◽  
Age Related

ObjectiveTo determine whether oxidative stress in virologically suppressed people with HIV (PWH) may contribute to or result from neurodegeneration, we measured 7,8-dihydro-8-oxoguanine (8-oxo-dG), a marker of DNA damage due to oxidative stress, and markers of age-related neurodegeneration, specifically, reduced levels of CSF Aβ-42, and elevated CSF total tau and neurofilament light (NFL).MethodsThis cross-sectional study prospectively enrolled participants at 6 US centers in the CNS HIV Antiretroviral Effects Research study. Inclusion criteria included HIV+ with a plasma level of HIV RNA ≤50 copies/mL. Exclusions included significant CNS confounding conditions. Measurements of total tau and Aβ-42 were performed by bead suspension array. NFL and 8-oxo-dG were measured using ELISA.ResultsParticipants were 53 PWH, mean age 55 (±9.3) years, 19% women, and 48% non-Hispanic White. Higher 8-oxo-dG correlated with markers of AD-related neurodegeneration including lower CSF Aβ-42 (r = −0.34; p = 0.012) and higher CSF NFL (r = 0.39; p = 0.0091) and total tau (r = 0.6696; p < 0.0001). Relationships remained after adjusting for demographic variables. Levels of protein carbonyls, a marker of protein oxidation, were not related to neurodegeneration markers.ConclusionsAmong virologically suppressed PWH, nucleic acid oxidation was associated with standard CSF biomarkers of neurodegeneration. Potential sources of oxidative stress in PWH include low-level HIV replication, inflammation, mitochondrial dysfunction, and specific antiretroviral drugs. Results suggest that the higher levels of oxidative stress among PWH may play a role in neurodegeneration.Classification of evidenceThis study provides Class II evidence that among virologically suppressed PWH, nucleic acid oxidation is associated with standard CSF biomarkers of neurodegeneration.

scholarly journals Oxidative Stress and Proteostasis Network: Culprit and Casualty of Alzheimer’s-Like Neurodegeneration

2014 ◽  
Vol 2014 ◽  
pp. 1-14 ◽  
Author(s):  
Fabio Di Domenico ◽  
Elizabeth Head ◽  
D. Allan Butterfield ◽  
Marzia Perluigi
Keyword(s):  
Oxidative Stress ◽  
Protein Oxidation ◽  
Neuronal Death ◽  
Protein Function ◽  
Protein Quality ◽  
Protective Role ◽  
Relevant Factor ◽  
Large Protein ◽  
Age Related

Free radical-mediated damage to proteins is particularly important in aging and age-related neurodegenerative diseases, because in the majority of cases it is a non-reversible phenomenon that requires clearance systems for removal. Major consequences of protein oxidation are loss of protein function and the formation of large protein aggregates, which are often toxic to cells if allowed to accumulate. Deposition of aggregated, misfolded, and oxidized proteins may also result from the impairment of protein quality control (PQC) system, including protein unfolded response, proteasome, and autophagy. Perturbations of such components of the proteostasis network that provides a critical protective role against stress conditions are emerging as relevant factor in triggering neuronal death. In this outlook paper, we discuss the role of protein oxidation as a major contributing factor for the impairment of the PQC regulating protein folding, surveillance, and degradation. Recent studies from our group and from others aim to better understand the link between Down syndrome and Alzheimer’s disease neuropathology. We propose oxidative stress and alteration of proteostasis network as a possible unifying mechanism triggering neurodegeneration.

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