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 ◽  
...  

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.

Antioxidants ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 29 ◽  
Author(s):  
Koichi Yada ◽  
Llion Arwyn Roberts ◽  
Natsumi Oginome ◽  
Katsuhiko Suzuki

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.


2021 ◽  
Vol 11 ◽  
Author(s):  
Anand Thirupathi ◽  
Ricardo A. Pinho ◽  
Ukadike C. Ugbolue ◽  
Yuhuan He ◽  
Yao Meng ◽  
...  

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.


2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Dimitrios Stagos ◽  
Nikolaos Goutzourelas ◽  
Amalia-Maria Ntontou ◽  
Ioannis Kafantaris ◽  
Chariklia K. Deli ◽  
...  

The aim of the present study was to investigate the use of static (sORP) and capacity ORP (cORP) oxidation-reduction potential markers as measured by the RedoxSYS Diagnostic System in plasma, for assessing eccentric exercise-induced oxidative stress. Nineteen volunteers performed eccentric exercise with the knee extensors. Blood was collected before, immediately after exercise, and 24, 48, and 72 h after exercise. Moreover, common redox biomarkers were measured, which were protein carbonyls, thiobarbituric acid-reactive substances, total antioxidant capacity in plasma, and catalase activity and glutathione levels in erythrocytes. When the participants were examined as one group, there were not significant differences in any marker after exercise. However, in 11 participants there was a high increase in cORP after exercise, while in 8 participants there was a high decrease. Thus, the participants were divided in low cORP group exhibiting significant decrease in cORP after exercise and in high cORP group exhibiting significant increase. Moreover, only in the low cORP group there was a significant increase in lipid peroxidation after exercise suggesting induction of oxidative stress. The results suggested that high decreases in cORP values after exercise may indicate induction of oxidative stress by eccentric exercise, while high increases in cORP values after exercise may indicate no existence of oxidative stress.


2005 ◽  
Vol 99 (4) ◽  
pp. 1434-1441 ◽  
Author(s):  
Ümit Kemal Şentürk ◽  
Filiz Gündüz ◽  
Oktay Kuru ◽  
Günnur Koçer ◽  
Yaşar Gül Özkaya ◽  
...  

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.


2019 ◽  
Vol 97 (Supplement_2) ◽  
pp. 181-181
Author(s):  
Carl A Frame ◽  
Logan R Kilburn ◽  
Erika M Johnson ◽  
Mariana C Rossoni Serao

Abstract Endogenous protein oxidation as a result of oxidative stress is known to reduce the efficiency of livestock species (Boler et al., 2012; DeRouchey et al., 2004; Dibner, Atwell, Kitchell, Shermer, & Ivey, 1996). Additionally, rendered by-products are common feedstuffs in livestock diets. During processing, these sources have the potential to become oxidized. While most research on oxidative stress has focused on consumption of dietary oxidized lipids, little research has been done in the area of dietary oxidized proteins and the potential to induce oxidative stress. The objective of this study was to determine the effects of dietary oxidized protein on oxidative stress in pigs. For this study, 30 pigs 6 weeks old were divided into three dietary treatments of control, medium, and high dietary oxidized protein. Each treatment was fed the same diet, with the exception of the degree of oxidation in bovine plasma which was included in the diet at 10 percent. Pigs were fed for 19 days and then euthanized for tissues collected. Jejunum, liver, and colon were collected along with urine and plasma samples on day 0 and 18. Jejunum samples were also collected for histology. Markers of oxidative stress included protein carbonyls, thiobarbituric acid reactive substance (TBARS), 8-hydroxyguanine, and glutathione peroxidase activity. Pigs in the high oxidation treatment had an increase in crypt depth of 16 percent (p-value less than 0.05) when compared to control further resulting in an 11 percent decrease in villi height to crypt depth ratio (p-value less than 0.05). Additionally, lipid oxidation products, measured by TBARS, was 28 percent greater in the liver of pigs in the medium oxidation treatment (p-value less than 0.05) when compared to control. Even with the short duration of this study, dietary oxidized protein did impact the oxidative status of the animal. Using pigs as a model for companion animals, it could be hypothesized then that long-term exposure could have implications on longevity.


Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 866
Author(s):  
Takaki Tominaga ◽  
Tsukasa Ikemura ◽  
Koichi Yada ◽  
Kazue Kanda ◽  
Kaoru Sugama ◽  
...  

Strenuous exercise induces organ damage, inflammation and oxidative stress. To prevent exercise-induced organ damage, inflammation and oxidative stress, rehydrating may be an effective strategy. In the present study, we aimed to examine whether beverage intake after exhaustive exercise to recover from dehydration prevents such disorders. Thirteen male volunteers performed incremental cycling exercise until exhaustion. Immediately after exercise, the subjects drank an electrolyte containing water (rehydrate trial: REH) or did not drink any beverage (control trial: CON). Blood samples were collected before (Pre), immediately (Post), 1 h and 2 h after exercise. Urine samples were also collected before (Pre) and 2 h after exercise. We measured biomarkers of organ damage, inflammation and oxidative stress in blood and urine. Biomarkers of muscle, renal and intestinal damage and inflammation increased in the blood and urine after exercise. However, changes in biomarkers of organ damage and inflammation did not differ between trials (p > 0.05). The biomarker of oxidative stress, thiobarbituric acid reactive substances (TBARS), in plasma, showed different changes between trials (p = 0.027). One hour after exercise, plasma TBARS concentration in REH had a higher trend than that in CON (p = 0.052), but there were no significant differences between Pre and the other time points in each trial. These results suggest that beverage intake after exercise does not attenuate exercise-induced organ damage, inflammation or oxidative stress in healthy males. However, rehydration restores exercise-induced oxidative stress more quickly.


1994 ◽  
Vol 77 (5) ◽  
pp. 2177-2187 ◽  
Author(s):  
C. K. Sen ◽  
M. Atalay ◽  
O. Hanninen

Glutathione (GSH) plays a central role in coordinating the synergism between different lipid- and aqueous-phase antioxidants. We documented 1) how exogenous GSH and N-acetylcysteine (NAC) may affect exhaustive exercise-induced changes in tissue GSH status, lipid peroxides [thiobarbituric acid-reactive substances (TBARS)], and endurance and 2) the relative role of endogenous GSH in the circumvention of exercise-induced oxidative stress by using GSH-deficient [L-buthionine-(S,R)-sulfoximine (BSO)-treated] rats. Intraperitoneal injection of GSH remarkably increased plasma GSH; exogenous GSH per se was an ineffective delivery agent of GSH to tissues. Repeated administration of GSH (1 time/day for 3 days) increased blood and kidney total GSH [TGSH; GSH+oxidized GSH (GSSG)]. Neither GSH nor NAC influenced endurance to exhaustion. NAC decreased exercise-induced GSH oxidation in the lung and blood. BSO decreased TGSH pools in the liver, lung, blood, and plasma by approximately 50% and in skeletal muscle and heart by 80–90%. Compared with control, resting GSH-deficient rats had lower GSSG in the liver, red gastrocnemius muscle, heart, and blood; similar GSSG/TGSH ratios in the liver, heart, lung, blood, and plasma; higher GSSG/TGSH ratios in the skeletal muscle; and more TBARS in skeletal muscle, heart, and plasma. In contrast to control, exhaustive exercise of GSH-deficient rats did not decrease TGSH in the liver, muscle, or heart or increase TGSH of plasma; GSSG of muscle, blood, or plasma; or TBARS of plasma or muscle. GSH-deficient rats had approximately 50% reduced endurance, which suggests a critical role of endogenous GSH in the circumvention of exercise-induced oxidative stress and as a determinant of exercise performance.


2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Efthalia Kerasioti ◽  
Dimitrios Stagos ◽  
Vasiliki Georgatzi ◽  
Erinda Bregou ◽  
Alexandros Priftis ◽  
...  

Excessive production of reactive oxygen species (ROS) may cause endothelial dysfunction and consequently vascular disease. In the present study, the possible protective effects of sheep whey protein (SWP) from tert-butyl hydroperoxide- (tBHP-) induced oxidative stress in endothelial cells (EA.hy926) were assessed using oxidative stress biomarkers. These oxidative stress biomarkers were glutathione (GSH) and ROS levels determined by flow cytometry. Moreover, thiobarbituric acid-reactive substances (TBARS), protein carbonyls (CARB), and oxidized glutathione (GSSG) were determined spectrophotometrically. The results showed that SWP at 0.78, 1.56, 3.12, and 6.24 mg of protein mL−1increased GSH up to 141%, while it decreased GSSG to 46.7%, ROS to 58.5%, TBARS to 52.5%, and CARB to 49.0%. In conclusion, the present study demonstrated for the first time that SWP protected endothelial cells from oxidative stress. Thus, SWP may be used for developing food supplements or biofunctional foods to attenuate vascular disturbances associated with oxidative stress.


1995 ◽  
Vol 79 (1) ◽  
pp. 129-135 ◽  
Author(s):  
Z. Radak ◽  
K. Asano ◽  
M. Inoue ◽  
T. Kizaki ◽  
S. Oh-Ishi ◽  
...  

A superoxide dismutase derivative (SM-SOD) that circulates and is bound to albumin with a half-life of 6 h was injected intraperitoneally into rats before exhaustive treadmill running to study its antioxidant scavenging capacity in the plasma and soleus and tibialis muscles. The exercise induced a marked increase in xanthine oxidase activity in plasma and an increase in thiobarbituric acid-reactive substances in the plasma as well as in the soleus and tibialis muscles of nonadministered rats immediately after the exercise. The immunoreactive content and activity of both SOD isoenzymes (Cu,Zn-SOD and Mn-SOD) of the nonadministered rats increased in the soleus and tibialis muscles immediately after running. SM-SOD treatment definitely attenuated the degree of the increase in thiobarbituric acid-reactive substances and xanthine oxidase in all samples examined immediately after exercise. Glutathione peroxidase activity significantly increased in the soleus muscle of nonadministered rats 1 day after running, whereas catalase activity remained unchanged throughout the experimental period. These results suggest that a single bout of exhaustive exercise induces oxidative stress in skeletal muscle of rats and that this oxidative stress can be attenuated by exogenous SM-SOD.


2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Lukasz Gwozdzinski ◽  
Anna Pieniazek ◽  
Joanna Bernasinska-Slomczewska ◽  
Pawel Hikisz ◽  
Krzysztof Gwozdzinski

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.


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