Little change in markers of protein breakdown and oxidative stress in humans in immobilization-induced skeletal muscle atrophy

2010 ◽  
Vol 35 (2) ◽  
pp. 125-133 ◽  
Author(s):  
Elisa I. Glover ◽  
Nobuo Yasuda ◽  
Mark A. Tarnopolsky ◽  
Arkan Abadi ◽  
Stuart M. Phillips
Keyword(s):  
Oxidative Stress ◽  
Caspase 3 ◽  
Oxidative Modification ◽  
Skeletal Muscle Atrophy ◽  
Protein Carbonyls ◽  
Disuse Atrophy ◽  
Protein Breakdown ◽  
Protein Conjugates ◽  
Protein Ubiquitination ◽  
And Oxidative Stress

A number of studies in rodents suggest that disuse atrophy results from a large increase in proteolysis affected by, or accompanying, increased oxidative stress. Little information is available, however, about the effects of immobilization on markers of muscle protein breakdown and oxidative stress in humans. Therefore, the purpose of this investigation was to measure markers of breakdown or oxidative stress in subjects who underwent 14 days of knee-brace-mediated immobilization. Vastus lateralis samples taken from 21 young subjects before, and 2 days and 14 days after, single leg immobilization were measured for ubiquitin-protein conjugates, caspase 3/7 activity, the 14-kDa caspase-3 cleaved actin fragment, 4-hydroxy-2-nonenal (4-HNE) adducts, and protein carbonyls. Quadriceps cross-sectional area decreased by 5.7% ± 1.1% (p < 0.0001) following immobilization. Ubiquitin-protein conjugates were elevated at 2 days of immobilization (12%, p < 0.05) but were not different from baseline at 14 days. Levels of the 14-kDa actin fragment and caspase 3/7 activity did not change over the immobilization period. The oxidative stress markers, 4-HNE adducts and protein carbonyls, did not change at any time point. These static measures of breakdown and oxidative modification suggest that a small increase in protein ubiquitination occurs early (2 days), but elevations in ubiquitinated or oxidatively modified proteins are not sustained during the later phase (14 days) of uncomplicated disuse atrophy in humans, suggesting that these pathways are not playing a major role in simple disuse-induced atrophic loss of protein mass.

scholarly journals Cytokines and Oxidative Stress Status Following a Handball Game in Elite Male Players

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Douglas Popp Marin ◽  
Rita de Cassia Macedo dos Santos ◽  
Anaysa Paola Bolin ◽  
Beatriz Alves Guerra ◽  
Elaine Hatanaka ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant System ◽  
Stress Responses ◽  
Oxidative Modification ◽  
Protein Carbonyls ◽  
Antioxidant Enzyme Activities ◽  
Oxidative Stress Biomarkers ◽  
Damage Indices ◽  
Plasma Antioxidant Capacity ◽  
And Oxidative Stress

Background. Handball is considered an intermittent sport that places an important stress on a player's aerobic and anaerobic metabolism. However, the oxidative stress responses following a handball game remain unknown. We investigated the responses of plasma and erythrocyte antioxidant system and oxidative stress biomarkers following a single handball game.Methods. Fourteen male elite Brazilian handball athletes were recruited in the present study. Blood samples were taken before, immediately, and 24 hours after the game.Results. After the game and during 24 hours of recovery, the concentration of all oxidative stress indices changed significantly in a way indicating increased oxidative stress in the blood (thiol groups and reduced glutathione decreased, whereas TBARS and plasma antioxidant capacity was increased) as well as in erythrocyte (increased levels of TBARS and protein carbonyls). Erythrocyte antioxidant enzyme activities were also significantly changed by handball. Muscle damage indices (creatine kinase and lactate dehydrogenase) increased significantly after exercise. In addition, IL-6 increased after the game, whereas TNF-αdecreased during recovery.Conclusion. This study demonstrates that a single handball game in elite athletes induces a marked state of oxidative stress evidenced by the oxidative modification in plasma and erythrocyte macromolecules, as well as by changes in the enzymatic and nonenzymatic antioxidant system.

Anaerobic Exercise and Oxidative Stress: A Review

2004 ◽  
Vol 29 (3) ◽  
pp. 245-263 ◽  
Author(s):  
Richard J. Bloomer ◽  
Allan H. Goldfarb
Keyword(s):  
Oxidative Stress ◽  
Exercise Training ◽  
Exercise Bout ◽  
Oxidative Modification ◽  
Anaerobic Exercise ◽  
Antioxidant Defenses ◽  
Protein Carbonyls ◽  
Anaerobic Work ◽  
Exercise Induced ◽  
And Oxidative Stress

Oxidative stress and subsequent damage to cellular proteins, lipids, and nucleic acids, as well as changes to the glutathione system, are well documented in response to aerobic exercise. However, far less information is available on anaerobic exercise-induced oxidative modifications. Recent evidence indicates that high intensity anaerobic work does result in oxidative modification to the above-mentioned macromolecules in both skeletal muscle and blood. Also, it appears that chronic anaerobic exercise training can induce adaptations that act to attenuate the exercise-induced oxidative stress. These may be specific to increased antioxidant defenses and/or may act to reduce the generation of pro-oxidants during and after exercise. However, a wide variety of exercise protocols and assay procedures have been used to study oxidative stress pertaining to anaerobic work. Therefore, precise conclusions about the exact extent and location of oxidative macromolecule damage, in addition to the adaptations resulting from chronic anaerobic exercise training, are difficult to indicate. This manuscript provides a review of anaerobic exercise and oxidative stress, presenting both the acute effects of a single exercise bout and the potential for adaptations resulting from chronic anaerobic training. Key words: antioxidants, free radicals, training, lipid peroxidation, protein carbonyls

246 Effects of Feeding Thermally Processed Spray-dried Egg Whites on Growth Performance, Apparent Digestibility, and Oxidative Stress in Nursery Pigs

2021 ◽  
Vol 99 (Supplement_1) ◽  
pp. 91-92
Author(s):  
Victoria C Wilson ◽  
Brian J Kerr
Keyword(s):  
Oxidative Stress ◽  
Growth Performance ◽  
Liver Tissue ◽  
Protein Carbonyls ◽  
Nursery Pigs ◽  
Thermally Processed ◽  
Markers Of Oxidative Stress ◽  
Dietary Treatments ◽  
And Oxidative Stress ◽  
Spray Dried

Abstract The objectives of this study were to determine if feeding thermally processed (TP, heated at 100°C for 120 h) spray-dried egg whites (SDEW) to nursery pigs would impact growth performance, apparent total tract digestibility (ATTD) of GE, N, and S, and oxidative stress. Thirty-two barrows, (initial BW 7.1 kg) were randomly assigned to dietary treatments with 1 pig per pen. In a preliminary study, thermally processing SDEW at 100°C for 120 h increased protein carbonyls (PC) from 6 µmol/g to 19.4 µmol/g (P ≤ 0.01). Diets included either 12% SDEW, 6% TP-SDEW plus 6% SDEW, or 12% TP-SDEW. The experiment lasted 24 d for collection of growth performance data, while plasma was collected on d 21 and liver tissue harvested on d 24 to analyze for markers of oxidative stress. Feces were collected on d 22 for measures of ATTD. Daily gain, daily feed intake, feed efficiency, and ATTD of GE were not found to be different among dietary treatments (P ≥ 0.57). In contrast, ATTD of N (P = 0.11) and S (P = 0.03) were found to increase with increasing protein oxidation in the diet. There was no change in the plasma or liver F2-isoprostanes and 8-hydroxy-2’-deoxyguanosine among dietary treatments (P ≥ 0.28). An increase in plasma PC (P = 0.02) was observed in pigs fed 12% TP-SDEW compared to pigs fed 12% SDEW and pigs fed 6% TP-SDEW. In contrast, a decrease in liver tissue PC (P = 0.04) was observed in pigs fed 6% TP-SDEW compared to pigs fed 12% SDEW and 12% TP-SDEW. These results indicate that feeding TP-SDEW does not affect growth performance, ATTD of GE, and oxidative stress as indicated by F2-isoprostanes or 8-hydroxy-2’-deoxyguanosine; but appeared to have variable effects on oxidative stress as measured by PC.

scholarly journals Manual Therapy Reduces Pain Behavior and Oxidative Stress in a Murine Model of Complex Regional Pain Syndrome Type I

2019 ◽  
Vol 9 (8) ◽  
pp. 197 ◽  
Author(s):  
Afonso S. I. Salgado ◽  
Juliana Stramosk ◽  
Daniela D. Ludtke ◽  
Ana C. C. Kuci ◽  
Daiana C. Salm ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Complex Regional Pain Syndrome ◽  
Manual Therapy ◽  
Pain Syndrome ◽  
Pain Behavior ◽  
Protein Carbonyls ◽  
Type I ◽  
Syndrome Type ◽  
Painful Condition ◽  
And Oxidative Stress

Complex regional pain syndrome type I (CRPS-I) is a chronic painful condition. We investigated whether manual therapy (MT), in a chronic post-ischemia pain (CPIP) model, is capable of reducing pain behavior and oxidative stress. Male Swiss mice were subjected to ischemia-reperfusion (IR) to mimic CRPS-I. Animals received ankle joint mobilization 48h after the IR procedure, and response to mechanical stimuli was evaluated. For biochemical analyses, mitochondrial function as well as oxidative stress thiobarbituric acid reactive substances (TBARS), protein carbonyls, antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) levels were determined. IR induced mechanical hyperalgesia which was subsequently reduced by acute MT treatment. The concentrations of oxidative stress parameters were increased following IR with MT treatment preventing these increases in malondialdehyde (MDA) and carbonyls protein. IR diminished the levels of SOD and CAT activity and MT treatment prevented this decrease in CAT but not in SOD activity. IR also diminished mitochondrial complex activity, and MT treatment was ineffective in preventing this decrease. In conclusion, repeated sessions of MT resulted in antihyperalgesic effects mediated, at least partially, through the prevention of an increase of MDA and protein carbonyls levels and an improvement in the antioxidant defense system.

Caspase-3-mediated cleavage of PHF-1 tau during apoptosis irrespective of excitotoxicity and oxidative stress: an implication to Alzheimer's disease

2005 ◽  
Vol 18 (3) ◽  
pp. 450-458 ◽  
Author(s):  
Hyo Jung Kang ◽  
Won Joo Yoon ◽  
Gyeong Joon Moon ◽  
Doo Yeon Kim ◽  
Seonghyang Sohn ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Caspase 3 ◽  
And Oxidative Stress

scholarly journals MiR-122 Participates in Oxidative Stress and Apoptosis in STZ-Induced Pancreatic β Cells by Regulating PI3K/AKT Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Jing Wang ◽  
Zhichun Dong ◽  
Liyin Lou ◽  
Lijuan Yang ◽  
Jingying Qiu
Keyword(s):  
Oxidative Stress ◽  
Insulin Secretion ◽  
Caspase 3 ◽  
Cell Damage ◽  
Caspase 9 ◽  
Intracellular Ros ◽  
Reverse Transcription Quantitative Pcr ◽  
Apoptosis Detection ◽  
Dichlorofluorescein Diacetate ◽  
And Oxidative Stress

At present, there are few reports concerning the relationship between miR-122 and diabetes. In addition, the effect of miR-122 on streptozotocin- (STZ-) induced oxidative damage in INS-1 cells remains unclear. The present study aimed to investigate the role and modulatory mechanisms involving miR-122 in diabetes. STZ was used to induce INS-1 cell damage. Reverse transcription-quantitative PCR was used to investigate the expression of miR-122. A TUNEL cell apoptosis detection kit was used to detect apoptosis. Intracellular ROS levels were determined using dichlorofluorescein-diacetate. The activities of insulin secretion, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-px) were measured using ELISA kits. Western blotting was used to measure the expression levels of Bax, Bcl-2, PI3K, p-PI3K, caspase-3 and caspase-9, cleaved-caspase-3 and cleaved-caspase-9, AKT, and p-AKT. Then, LY294002 (LY, PI3K inhibitor) was used to treat INS-1 cells, and oxidative stress and apoptosis were measured. The results showed that STZ-induced inhibitory effects on insulin secretion were mitigated by miR-122 inhibitor, and the activities of SOD, CAT, and GSH-px were also increased. Furthermore, miR-122 inhibitor inhibited apoptosis and oxidative stress in STZ-induced INS-1 cells. Finally, the addition of LY increased insulin levels; reduced the activities of SOD, CAT, and GSH-px; and promoted apoptosis in STZ-induced INS-1 cells. In conclusion, interference with miR-122 can inhibit oxidative stress and apoptosis in STZ-induced INS-1 cells, involving a mechanism of action related to the PI3K/AKT pathway.

scholarly journals Methyl Jasmonate Reduces Inflammation and Oxidative Stress in the Brain of Arthritic Rats

Antioxidants ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 485 ◽  
Author(s):  
Pereira-Maróstica ◽  
Castro ◽  
Gonçalves ◽  
Silva ◽  
Bracht ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Methyl Jasmonate ◽  
Lipid Peroxides ◽  
Mitochondrial Respiratory Chain ◽  
Antioxidant Defenses ◽  
Protein Carbonyls ◽  
Partial Recovery ◽  
Negative Effects ◽  
The Brain ◽  
And Oxidative Stress

Methyl jasmonate (MeJA), common in the plant kingdom, is capable of reducing articular and hepatic inflammation and oxidative stress in adjuvant-induced arthritic rats. This study investigated the actions of orally administered MeJA (75–300 mg/kg) on inflammation, oxidative stress and selected enzyme activities in the brain of Holtzman rats with adjuvant-induced arthritis. MeJA prevented the arthritis-induced increased levels of nitrites, nitrates, lipid peroxides, protein carbonyls and reactive oxygen species (ROS). It also prevented the enhanced activities of myeloperoxidase and xanthine oxidase. Conversely, the diminished catalase and superoxide dismutase activities and glutathione (GSH) levels caused by arthritis were totally or partially prevented. Furthermore, MeJA increased the activity of the mitochondrial isocitrate dehydrogenase, which helps to supply NADPH for the mitochondrial glutathione cycle, possibly contributing to the partial recovery of the GSH/oxidized glutathione (GSSG) ratio. These positive actions on the antioxidant defenses may counterbalance the effects of MeJA as enhancer of ROS production in the mitochondrial respiratory chain. A negative effect of MeJA is the detachment of hexokinase from the mitochondria, which can potentially impair glucose phosphorylation and metabolism. In overall terms, however, it can be concluded that MeJA attenuates to a considerable extent the negative effects caused by arthritis in terms of inflammation and oxidative stress.

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