Exercise-induced oxidative stress leads hemolysis in sedentary but not trained humans

2005 ◽  
Vol 99 (4) ◽  
pp. 1434-1441 ◽  
Author(s):  
Ümit Kemal Şentürk ◽  
Filiz Gündüz ◽  
Oktay Kuru ◽  
Günnur Koçer ◽  
Yaşar Gül Özkaya ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Osmotic Fragility ◽  
Thiobarbituric Acid ◽  
Protein Carbonyl ◽  
Antioxidant Vitamin ◽  
Thiobarbituric Acid Reactive Substance ◽  
Protein Carbonyl Content ◽  
Trained Subjects ◽  
Exercise Induced ◽  
Sedentary Subjects

Intravascular hemolysis is one of the most emphasized mechanisms for destruction of erythrocytes during and after physical activity. Exercise-induced oxidative stress has been proposed among the different factors for explaining exercise-induced hemolysis. The validity of oxidative stress following exhaustive cycling exercise on erythrocyte damage was investigated in sedentary and trained subjects before and after antioxidant vitamin treatment (A, C, and E) for 2 mo. Exercise induced a significant increase in thiobarbituric acid-reactive substance and protein carbonyl content levels in sedentary subjects and resulted in an increase of osmotic fragility and decrease in deformability of erythrocytes, accompanied by signs for intravascular hemolysis (increase in plasma hemoglobin concentration and decrease in haptoglobulin levels). Administration of antioxidant vitamins for 2 mo prevented exercise-induced oxidative stress (thiobarbituric acid-reactive substance, protein carbonyl content) and deleterious effects of exhaustive exercise on erythrocytes in sedentary subjects. Trained subjects' erythrocyte responses to exercise were different from those of sedentary subjects before antioxidant vitamin treatment. Osmotic fragility and deformability of erythrocytes, plasma hemoglobin concentration, and haptoglobulin levels were not changed after exercise, although the increased oxidative stress was observed in trained subjects. After antioxidant vitamin treatment, functional and structural parameters of erythrocytes were not altered in the trained group, but exercise-induced oxidative stress was prevented. Increased percentage of young erythrocyte populations was determined in trained subjects by density separation of erythrocytes. These findings suggest that the exercise-induced oxidative stress may contribute to exercise-induced hemolysis in sedentary humans.

scholarly journals Effect of Running Exercise on Oxidative Stress Biomarkers: A Systematic Review

2021 ◽  
Vol 11 ◽  
Author(s):  
Anand Thirupathi ◽  
Ricardo A. Pinho ◽  
Ukadike C. Ugbolue ◽  
Yuhuan He ◽  
Yao Meng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Thiobarbituric Acid ◽  
Protein Carbonyl ◽  
Enzymatic Antioxidants ◽  
Oxidative Stress Biomarkers ◽  
Running Exercise ◽  
Exercise Induced ◽  
The Individual ◽  
Meta Analyses

Background: Exercise induced health benefits are limited by the overaccumulation of reactive oxygen species (ROS). ROS and further oxidative stress could potentially induce muscle damage which could result in poor exercise performance. However, predicting ROS induced oxidative stress in response to endurance training has several limitations in terms of selecting biomarkers that are used to measure oxidative stress.Objective: The purpose of this study was to systematically investigate the suitable biomarkers that predict oxidative stress status among runners.Methods: According to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement, a search for relevant articles was carried out on PubMed/Medline, ISI Web of Science, and Google Scholar using related search terms such as oxidative damage, ROS, exercise, physical training, running, marathon, and ultramarathon.Results: Outcomes included (1) running programs like a half-marathon, ultramarathon, and iron-man race, (2) measuring biochemical assessment of oxidative damage markers such as malondialdehyde (MDA), protein carbonyl (PC), total antioxidant capacity (TAC), thiobarbituric acid reactive substances (TBARS), 8-Oxo-2'-deoxyguanosine (8-OH-dG), 4-hydroxynonenal (HNE), and F1-isoprostones, and enzymatic and non-enzymatic antioxidants level.Conclusions: This study concluded that a running exercise does not elicit a response to specific biomarkers of oxidative stress, instead, oxidative damage markers of lipids, proteins, and various enzymatic and non-enzymatic antioxidants are expressed according to the training status of the individual.

Potential sources of oxidative stress that induce postexercise proteinuria in rats

2008 ◽  
Vol 104 (4) ◽  
pp. 1063-1068 ◽  
Author(s):  
Günnur Koçer ◽  
Ümit Kemal Şentürk ◽  
Oktay Kuru ◽  
Filiz Gündüz
Keyword(s):  
Oxidative Stress ◽  
Nadph Oxidase ◽  
Oxidase Activity ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Protein Carbonyl ◽  
Exhaustive Exercise ◽  
Carbonyl Content ◽  
Protein Carbonyl Content ◽  
Nadph Oxidase Activity ◽  
Exercise Induced

Exercise-induced proteinuria is a common consequence of physical activity and is caused predominantly by alterations in renal hemodynamics. Although it has been shown that exercise-induced oxidative stress can also contribute to the occurrence of postexercise proteinuria, the sources of reactive oxygen species that promote it are unknown. We investigated the enzymes nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and xanthine oxidase (XO) as possible sources of oxidative stress in postexercise proteinuria. First, we evaluated the effect of blocking the NADPH oxidase enzyme on postexercise proteinuria. We found a significant increase in urinary protein level, kidney thiobarbituric acid-reactive substances (TBARS), and protein carbonyl content after exhaustive exercise, and NADPH oxidase activity was induced by exercise. Rats that were treated with an NADPH oxidase inhibitor for 4 days before exhaustive exercise showed no increase in kidney TBARS or protein carbonyl derivative level and no proteinuria or NADPH oxidase activation. In the next set of experiments, we investigated the effect of XO blockage on postexercise proteinuria. Oxypurinol, an XO inhibitor was administered to rats for 3 days before exercise. Although XO inhibition significantly decreased kidney TBARS levels and protein carbonyl content in exercised rats, the inhibition did not prevent exercise-induced proteinuria. However, plasma and kidney XO activity was not induced by exercise, but rather it was suppressed under oxypurinol treatment. These results suggest that increased NADPH oxidase activity induced by exhaustive exercise is an important source of elevated oxidative, stress during exercise, which contributes to the occurrence of postexercise proteinuria.

Diallyl trisulfide ameliorates arsenic-induced hepatotoxicity by abrogation of oxidative stress, inflammation, and apoptosis in rats

2014 ◽  
Vol 34 (5) ◽  
pp. 506-525 ◽  
Author(s):  
NC Sumedha ◽  
S Miltonprabu
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Protein Oxidation ◽  
Structural Changes ◽  
Histopathological Examination ◽  
Thiobarbituric Acid ◽  
Hepatic Function ◽  
Protein Carbonyl ◽  
Thiobarbituric Acid Reactive Substance ◽  
Diallyl Trisulfide

The present study investigates the possible ameliorative effects of diallyl trisulfide (DATS) against arsenic (As)-induced hepatotoxicity and oxidative stress in rats. The four experimental groups evaluated include: (1) vehicle control; (2) As (5 mg/kg/day); (3) DATS (80 mg/kg/day) + As; and (4) DATS. Induction of As in rats caused severe hepatotoxicity as evidenced by an elevation of serum aspartate aminotransferase and alanine aminotransferase activities and increased total bilirubin concentration, indicating hepatic function abnormalities. Histopathological examination revealed various structural changes in the liver, characterized by hepatocyte degeneration/necrosis, congestion, sinusoidal dilatation, vacuolation, and inflammatory cell infiltration. The significant decrease in reduced glutathione content, catalase, superoxide dismutase, glutathione peroxidase, and glutathione reductase activities and the significant increase in lipid peroxidation (thiobarbituric acid reactive substance) and protein oxidation (protein carbonyl) contents indicated that As-induced hepatotoxicity was mediated through oxidative stress. As intoxication also elevated the levels of Cas-3 and nitric oxide and increased the expression of nuclear factor-κB p65 in the liver. In contrast, DATS pretreatment significantly improved As-induced serum biochemical, immunohistochemical, and histopathological alterations reflecting hepatic dysfunction. These results may contribute to a better understanding of the hepatoprotective role of DATS, emphasizing the influence of this garlic trisulfide in the diet for human health, possibly preventing the hepatic injury associated with As intoxication, presumably due to its ability to inhibit lipid peroxidation, protein oxidation, and restoration of antioxidant status.

scholarly journals Ginsenoside-Rg1 Protects the Liver against Exhaustive Exercise-Induced Oxidative Stress in Rats

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Mallikarjuna Korivi ◽  
Chien-Wen Hou ◽  
Chih-Yang Huang ◽  
Shin-Da Lee ◽  
Ming-Fen Hsu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Thiobarbituric Acid ◽  
Exhaustive Exercise ◽  
Protein Carbonyls ◽  
Regular Exercise ◽  
Thiobarbituric Acid Reactive Substance ◽  
Ginsenoside Rg1 ◽  
Exercise Induced ◽  
First Time

Despite regular exercise benefits, acute exhaustive exercise elicits oxidative damage in liver. The present study determined the hepatoprotective properties of ginsenoside-Rg1 against exhaustive exercise-induced oxidative stress in rats. Forty rats were assigned into vehicle and ginsenoside-Rg1 groups (0.1 mg/kg bodyweight). After 10-week treatment, ten rats from each group performed exhaustive swimming. Estimated oxidative damage markers, including thiobarbituric acid reactive substance (TBARS) (67%) and protein carbonyls (56%), were significantly (P<0.01) elevated after exhaustive exercise but alleviated in ginsenoside-Rg1 pretreated rats. Furthermore, exhaustive exercise drastically decreased glutathione (GSH) content (∼79%) with concurrent decreased superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities. However, these changes were attenuated in Rg1 group. Additionally, increased xanthine oxidase (XO) activity and nitric oxide (NO) levels after exercise were also inhibited by Rg1 pretreatment. For the first time, our findings provide strong evidence that ginsenoside-Rg1 can protect the liver against exhaustive exercise-induced oxidative damage.

scholarly journals Alterations in the Plasma and Red Blood Cell Properties in Patients with Varicose Vein: A Pilot Study

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Lukasz Gwozdzinski ◽  
Anna Pieniazek ◽  
Joanna Bernasinska-Slomczewska ◽  
Pawel Hikisz ◽  
Krzysztof Gwozdzinski
Keyword(s):  
Oxidative Stress ◽  
Varicose Vein ◽  
Ache Activity ◽  
Plasma Membranes ◽  
Varicose Veins ◽  
Blood Stasis ◽  
Thiobarbituric Acid ◽  
Protein Carbonyl ◽  
Protein Carbonyls ◽  
Thiobarbituric Acid Reactive Substance

The varicose vein results from the inefficient functioning of the valves in the lower limb veins, making the blood flow slow down and leading to blood stasis and hypoxia. This type of vein dysfunction might be a result of the development of oxidative stress. We compared oxidative stress markers in the plasma and erythrocytes obtained from peripheral veins and varicose veins in the same patients (glutathione, nonenzymatic antioxidant capacity (NEAC), catalase (CAT) and acetylcholinesterase (AChE) activity, thiols, thiobarbituric acid-reactive substance (TBARS), and protein carbonyls). We found a decrease in NEAC in the plasma obtained from the varicose veins compared to the peripheral veins. We detected a decrease in thiols in the plasma, hemolysate, and plasma membranes and increase in protein carbonyl compounds and TBARS levels in the varicose veins. These changes were accompanied by a decrease in CAT and AChE activity. For the first time, our results show changes in the plasma, erythrocyte membrane, and hemolysate protein properties in varicose vein blood in contrast to the plasma and erythrocytes in peripheral vein blood from the same patients. The increased oxidative stress accompanying varicose vein disease might result from the local inefficiency of the antioxidant defense system.

scholarly journals Effect of Acacia Polyphenol Supplementation on Exercise-Induced Oxidative Stress in Mice Liver and Skeletal Muscle

Antioxidants ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 29 ◽  
Author(s):  
Koichi Yada ◽  
Llion Arwyn Roberts ◽  
Natsumi Oginome ◽  
Katsuhiko Suzuki
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Muscle Protein ◽  
Thiobarbituric Acid ◽  
Exhaustive Exercise ◽  
Protein Carbonyls ◽  
High Dose ◽  
Thiobarbituric Acid Reactive Substance ◽  
Skeletal Muscle Protein ◽  
Exercise Induced

The purpose of this study was to investigate the effects of acacia polyphenol (AP) supplementation on exercise-induced oxidative stress in mouse liver and skeletal muscle. Plasma aspartate aminotransferase (AST), liver and skeletal muscle levels of thiobarbituric acid reactive substance (TBARS), and levels of skeletal muscle protein carbonyls increased immediately after exhaustive exercise. Exhaustive exercise also decreased liver glutathione (GSH). These results suggest that the exhaustive exercise used in this study induced tissue damage and oxidative stress. Contrary to our expectations, AP supplementation increased plasma AST and alanine aminotransferase activities, liver levels of TBARS, and protein carbonyls. Furthermore, AP supplementation decreased glutathione and glutathione peroxidase activity in the liver. On the other hand, AP supplementation decreased TBARS levels in skeletal muscle. These results suggest that oral high-dose AP administration decreased oxidative stress in skeletal muscle but induced oxidative stress in the liver and increased hepatotoxicity.

Resistance of erythrocytes from Brown trout (Salmo trutta m. trutta L.) affected by ulcerative dermal necrosis syndrome

2011 ◽  
Vol 14 (3) ◽  
pp. 443-448 ◽  
Author(s):  
N. Kurhalyuk ◽  
H. Tkachenko ◽  
K. Pałczyńska
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Brown Trout ◽  
Salmo Trutta ◽  
Thiobarbituric Acid ◽  
Control Group ◽  
Thiobarbituric Acid Reactive Substance ◽  
Tbars Level ◽  
Reactive Substance ◽  
Brown Trout Salmo Trutta

Resistance of erythrocytes from Brown trout (Salmo trutta m. trutta L.) affected by ulcerative dermal necrosis syndrome In the present work we evaluated the effect of ulcerative dermal necrosis (UDN) syndrome on resistance of erythrocytes to haemolytic agents and lipid peroxidation level in the blood from brown trout (Salmo trutta m. trutta L.). Results showed that lipid peroxidation increased in erythrocytes, as evidenced by high thiobarbituric acid reactive substance (TBARS) levels. Compared to control group, the resistance of erythrocytes to haemolytic agents was significantly lower in UDN-positive fish. Besides, UDN increased the percent of hemolysated erythrocytes subjected to the hydrochloric acid, urea and hydrogen peroxide. Results showed that UDN led to an oxidative stress in erythrocytes able to induce enhanced lipid peroxidation level, as suggested by TBARS level and decrease of erythrocytes resistance to haemolytic agents.

Role of Quercetin in Mitigation of Lindane Induced Toxicity in Terms of Oxidative Responses and Metabolic Status in Mice Brain

2020 ◽  
Vol 16 ◽  
Author(s):  
Anupama Sharma ◽  
Renu Bist ◽  
Hemant Pareek
Keyword(s):  
Citrate Synthase ◽  
Thiobarbituric Acid ◽  
Tca Cycle ◽  
Treated Group ◽  
Protein Carbonyl ◽  
Protein Carbonyl Content ◽  
Mice Brain ◽  
The Brain ◽  
Oxidative Responses

Background:: Current study evaluated the protective potential of quercetin against lindane induced toxicity in mice brain. For investigation, mice were allocated into four groups; First group was control. Second group was administered with oral dose of lindane (25 mg/kg bw) for 4 consecutive days. Third group was exposed to quercetin (40 mg/kg bw) and in fourth group, quercetin was administered 1 hour prior to the exposure of lindane. Objective:: Two major objectives were decided for study. First was to create lesions in the brain by lindane and; second was to evaluate the neuroprotective potential of quercetin. Methods:: To study oxidative responses, level of thiobarbituric acid reactive substances (TBARS), protein carbonyl content (PCC), reduced glutathione (GSH), superoxide dismutase (SOD), Catalase (CAT), and glutathione peroxidase (GPx) were measured in brain homogenates. Three key step regulating enzymes of tricarboxylic acid (TCA) cycle viz citrate synthase (CS), pyruvate dehydrogenase (PDH) and fumarase were also assayed. Results:: Lindane treatment significantly enhanced the levels of TBARS (P<0.001),PCC (P<0.001), GPx (P<0.001), SOD (P<0.05), PDH (P<0.05) and fumarase (P<0.001) in brains of mice compared to control. Meanwhile, it alleviated GSH, CAT and CS (P<0.05) activity. Conclusion:: Pretreatment with quercetin in lindane treated group not only restored, previously altered biochemical parameters after lindane treatment and also significantly improved them too which suggests that quercetin is not only invulnerable rather neuroprotective against lindane intoxication.

Alteration in the oxidative status of Drosophila melanogaster Meigen (Diptera: Drosophilidae) fed with a diet containing Centaurea depressa M. Bieb. (Asteraceae)

2020 ◽  
Vol 70 (2) ◽  
pp. 227-237
Author(s):  
Eda Güneş
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Antioxidant Enzymes ◽  
Total Protein ◽  
Protein Carbonyl ◽  
Control Group ◽  
Carbonyl Content ◽  
Protein Carbonyl Content ◽  
Freeze Dried ◽  
Dried Extract

Abstract The aim of the this study was to evaluate the effects of fresh, dried and freeze-dried Centaurea depressa M. Bieb. (Asteraceae) on the oxidant and antioxidant status of the model organism D. melanogaster Meigen (Diptera: Drosophilidae) experimentally. The study was carried out from 2016 to 2019, and plant leaf extracts (0-50 mg/l) were added to insect standard artificial diets. The total protein, protein carbonyl content and glutathione-S-transferase, superoxide dismutase and catalase activities were quantified at the insect’s third larval stage. Our data showed that protein carbonyl content varied from 2.70 nmol/mg protein in the control group to 59.11 nmol/mg protein in the group fed with fresh leaf extract signifying induction of oxidative stress. All extracts increased the levels of all antioxidant enzymes and decreased the amounts of total protein. Meanwhile, the group fed with the freeze-dried extract showed no significant difference in the levels of total protein and protein carbonyl content except at the 50 mg/l concentration of the extract. Moreover, this group had superoxide dismutase and catalase activities 4 to 5 times higher than in the control group. In conclusion, induction of oxidative stress indicates that the fresh form of C. depressa leaves may have potential as a natural pesticide, whereas induction of endogenous antioxidant enzymes by the freeze-dried extract suggest its potential as an antioxidant.

scholarly journals TUALANG HONEY ATTENUATES KAINIC ACID-INDUCED OXIDATIVE STRESS IN RAT CEREBELLUM AND BRAINSTEM

2017 ◽  
Vol 9 (12) ◽  
pp. 155 ◽  
Author(s):  
Nur Shafika Mohd Sairazi ◽  
K. N. S. Sirajudeen ◽  
Mustapha Muzaimi ◽  
Mummedy Swamy ◽  
Mohd Asnizam Asari ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Total Antioxidant Status ◽  
Thiobarbituric Acid ◽  
Protein Carbonyl ◽  
Multiple Time ◽  
Rat Cerebellum ◽  
Total Antioxidant ◽  
Multiple Time Points ◽  
Tualang Honey

Objective: The present study examined the protective effect of tualang honey (TH) against kainic acid (KA)-induced oxidative stress in the cerebellum and brainstem of rats.Methods: Male Sprague-Dawley rats were randomly divided into four groups: Control, KA-treated, TH+KA-treated, and topiramate (TPM, an antiepileptic agent)+KA-treated groups. Rats were pretreated orally with drinking water, TH (1.0 g/kg body weight), or TPM (40 mg/kg body weight), respectively, five times at 12 h intervals. Saline or KA (15 mg/kg body weight) were injected subcutaneously 30 min after last oral treatment. Rats were sacrificed at 2 h, 24 h, and 48 h after KA administration. Oxidative stress markers were analyzed in different brain regions (cerebellum and brainstem) 2 h, 24 h, and 48 h after KA administration.Results: KA caused significant (p<0.05) elevation in the thiobarbituric acid reactive substances level, protein carbonyl contents, and nitric oxide production, impairment of glutathione system, and a significant reduction in the total antioxidant status in the rat cerebellum and brainstem at multiple time-points, as compared to control groups. Pretreatment with TH significantly (p<0.05) reduced the elevation in the thiobarbituric acid reactive substances level, protein carbonyl contents, and nitric oxide production and increasing a reduction in the total antioxidant status in the rat cerebellum and brainstem induced by KA at multiple time-points, as compared to KA only-treated group.Conclusion: Taken together, this study suggests that TH has therapeutic potential in reducing oxidative stress in the cerebellum and brainstem of KA-induced rats via its antioxidant property.

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