scholarly journals Protective Effects of Sulforaphane on Exercise-Induced Organ Damage via Inducing Antioxidant Defense Responses

Antioxidants ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 136 ◽  
Author(s):  
Ruheea Taskin Ruhee ◽  
Sihui Ma ◽  
Katsuhiko Suzuki
Keyword(s):  
Oxidative Stress ◽  
Mrna Expression ◽  
Antioxidant Defense ◽  
Defense Responses ◽  
Organ Damage ◽  
Exercise Group ◽  
Exhaustive Exercise ◽  
Protective Effects ◽  
Antioxidant Defense Enzymes ◽  
Exercise Induced

Regular exercise is beneficial to maintain a healthy lifestyle, but the beneficial effects are lost in the case of acute exhaustive exercise; this causes significant inflammation, oxidative stress along with organ damage. Recently, sulforaphane (SFN), an indirect antioxidant, has drawn special attention for its potential protective effect against inflammation and oxidative stress. However, no studies have been performed regarding acute exhaustive exercise-induced organ damage in association with SFN administration. Therefore, the aim of this study was to investigate the effects of SFN on acute exhaustive exercise-induced organ damage and the mechanisms involved. To perform the study, we divided mice into four groups: Control, SFN, exercise, and SFN plus exercise. The SFN group was administered orally (50 mg/kg body wt) 2 h before the running test. We measured plasma levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH), and acute exhaustive exercise significantly increased these biomarkers. In addition, the mRNA expression of pro-inflammatory cytokines, IL-6, IL-1β, and TNF-α, were significantly increased in the liver of exercise group. However, the SFN plus exercise group showed a significant reduction in the expression of cytokines and blood biomarkers of tissue damage or cell death. Furthermore, we measured mRNA expression of Nrf2, heme oxygenase (HO)-1, and antioxidant defense enzymes expression, i.e., superoxide dismutase (SOD1), catalase (CAT), and glutathione peroxidase (GPx1) in the liver. The expression of all these biomarkers was significantly upregulated in the SFN plus exercise group. Collectively, SFN may protect the liver from exhaustive exercise-induced inflammation via inducing antioxidant defense response through the activation of Nrf2/HO-1 signal transduction pathway.

scholarly journals Characterization and Modulation of Systemic Inflammatory Response to Exhaustive Exercise in Relation to Oxidative Stress

Antioxidants ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 401 ◽  
Author(s):  
Katsuhiko Suzuki ◽  
Takaki Tominaga ◽  
Ruheea Taskin Ruhee ◽  
Sihui Ma
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Mediator ◽  
Inflammatory Responses ◽  
Organ Damage ◽  
Exhaustive Exercise ◽  
Nuclear Factor ◽  
Internal Organs ◽  
Research Findings ◽  
Exercise Induced

Exhaustive exercise induces systemic inflammatory responses, which are associated with exercise-induced tissue/organ damage, but the sources and triggers are not fully understood. Herein, the basics of inflammatory mediator cytokines and research findings on the effects of exercise on systemic inflammation are introduced. Subsequently, the association between inflammatory responses and tissue damage is examined in exercised and overloaded skeletal muscle and other internal organs. Furthermore, an overview of the interactions between oxidative stress and inflammatory mediator cytokines is provided. Particularly, the transcriptional regulation of redox signaling and pro-inflammatory cytokines is described, as the activation of the master regulatory factor nuclear factor (erythroid-derived 2)-like 2 (Nrf2) is involved directly or indirectly in controlling pro-inflammatory genes and antioxidant enzymes expression, whilst nuclear factor-kappa B (NF-κB) regulates the pro-inflammatory gene expression. Additionally, preventive countermeasures against the pathogenesis along with the possibility of interventions such as direct and indirect antioxidants and anti-inflammatory agents are described. The aim of this review is to give an overview of studies on the systematic inflammatory responses to exercise, including our own group as well as others. Moreover, the challenges and future directions in understanding the role of exercise and functional foods in relation to inflammation and oxidative stress are discussed.

scholarly journals The Effects of Beverage Intake after Exhaustive Exercise on Organ Damage, Inflammation and Oxidative Stress in Healthy Males

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 866
Author(s):  
Takaki Tominaga ◽  
Tsukasa Ikemura ◽  
Koichi Yada ◽  
Kazue Kanda ◽  
Kaoru Sugama ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Thiobarbituric Acid ◽  
Organ Damage ◽  
Exhaustive Exercise ◽  
Strenuous Exercise ◽  
Intestinal Damage ◽  
Urine Biomarkers ◽  
Exercise Induced ◽  
And Oxidative Stress ◽  
Healthy Males

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.

scholarly journals Total Dietary Antioxidant Intake Including Polyphenol Content: Is It Capable to Fight against Increased Oxidants within the Body of Ultra-Endurance Athletes?

Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1877
Author(s):  
Aslı Devrim-Lanpir ◽  
Pelin Bilgic ◽  
Tuğba Kocahan ◽  
Gökhan Deliceoğlu ◽  
Thomas Rosemann ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Exercise Performance ◽  
Antioxidant Defense ◽  
Endurance Athletes ◽  
Exhaustive Exercise ◽  
Dietary Antioxidant ◽  
Antioxidant Intake ◽  
Total Antioxidant ◽  
Exercise Induced ◽  
Ultra Endurance

The role of dietary antioxidants on exhaustive exercise-induced oxidative stress has been well investigated. However, the contribution of total dietary antioxidant capacity on exogenous antioxidant defense and exercise performance has commonly been disregarded. The aims of the present investigation were to examine (i) the effects of dietary total antioxidant intake on body antioxidant mechanisms, and (ii) an exhaustive exercise-induced oxidative damage in ultra-endurance athletes. The study included 24 ultra-marathon runners and long-distance triathletes (12 male and 12 female) who underwent an acute exhaustive exercise test (a cycle ergometer (45 min at 65% VO2max) immediately followed by a treadmill test (75% VO2max to exhaustion). Oxidative stress-related biomarkers (8-isoprostaglandin F2alpha (8-iso PGF2a), total oxidant status (TOS, total antioxidant status (TAS)) in plasma were collected before and after exercise. Oxidative stress index was calculated to assess the aspect of redox balance. Blood lactate concentrations and heart rate were measured at the 3rd and 6th min after exercise. Dietary antioxidant intake was calculated using the ferric reducing ability of plasma (FRAP) assay. Dietary total antioxidant intake of the subjects was negatively correlated with pre-exercise TOS concentrations (rs = −0.641 in male, and rs = −0.741 in females) and post- vs. pre- (∆) 8-iso PGF2a levels (rs = −0.702 in male; p = 0.016, and rs = −0.682 in females; p = 0.024), and positively correlated with ∆ TAS concentrations (rs = 0.893 in males; p = 0.001, and rs = 0.769 in females; p = 0.002) and post- exercise lactate concentrations (rs = 0.795 for males; p = 0.006, and rs = 0.642 for females; p = 0.024). A positive meaningful (p = 0.013) interaction was observed between time at exhaustion and dietary antioxidant intake (rs = 0.692) in males, but not in females. In conclusion, the determination of total dietary antioxidant intake in ultra-endurance athletes may be crucial for gaining a better perspective on body antioxidant defense against exhaustive exercise-induced oxidative stress. However, the effects of dietary antioxidant on exercise performance and recovery rate needs further investigation.

l-Arginine supplementation improves antioxidant defenses through l-arginine/nitric oxide pathways in exercised rats

2013 ◽  
Vol 115 (8) ◽  
pp. 1146-1155 ◽  
Author(s):  
Lingling Shan ◽  
Bin Wang ◽  
Guizhen Gao ◽  
Wengen Cao ◽  
Yunkun Zhang
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Physical Exercise ◽  
Endurance Training ◽  
Antioxidant Defense ◽  
Exhaustive Exercise ◽  
Antioxidant Defenses ◽  
Sedentary Control ◽  
Antioxidant Defense Capacity ◽  
Exercise Induced

l-Arginine (l-Arg) supplementation has been shown to enhance physical exercise capacity and delay onset of fatigue. This work investigated the potential beneficial mechanism(s) of l-Arg supplementation by examining its effect on the cellular oxidative and nitrosative stress pathways in the exercised rats. Forty-eight rats were randomly divided into six groups: sedentary control; sedentary control with l-Arg treatment; endurance training (daily swimming training for 8 wk) control; endurance training with l-Arg treatment; an exhaustive exercise (one time swimming to fatigue) control; and an exhaustive exercise with l-Arg treatment. l-Arg (500 mg/kg body wt) or saline was given to rats by intragastric administration 1 h before the endurance training and the exhaustive swimming test. Expression levels and activities of the l-Arg/nitric oxide (NO) pathway components and parameters of the oxidative stress and antioxidant defense capacity were investigated in l-Arg-treated and control rats. The result show that the l-Arg supplementation completely reversed the exercise-induced activation of NO synthase and superoxide dismutase, increased l-Arg transport capacity, and increased NO and anti-superoxide anion levels. These data demonstrate that l-Arg supplementation effectively reduces the exercise-induced imbalance between oxidative stress and antioxidant defense capacity, and this modulation is likely mediated through the l-Arg/NO pathways. The findings of this study improved our understanding of how l-Arg supplementation prevents elevations of reactive oxygen species and favorably enhances the antioxidant defense capacity during physical exercise.

scholarly journals Protective Effects of GYY4137 on Renal Ischaemia/Reperfusion Injury through Nrf2-Mediated Antioxidant Defence

2021 ◽  
pp. 1-9
Author(s):  
Hongmei Zhao ◽  
Yun Qiu ◽  
Yichen Wu ◽  
Hong Sun ◽  
Sumin Gao
Keyword(s):  
Oxidative Stress ◽  
Reperfusion Injury ◽  
Nuclear Translocation ◽  
Organ Damage ◽  
Related Factor ◽  
Protective Effects ◽  
Ischaemia Reperfusion Injury ◽  
Renal Ischaemia ◽  
Ischaemia Reperfusion ◽  
Renal Histology

<b><i>Introduction/Aims:</i></b> Hydrogen sulfide (H<sub>2</sub>S) is considered to be the third most important endogenous gasotransmitter in organisms. GYY4137 is a long-acting donor for H<sub>2</sub>S, a gas transmitter that has been shown to prevent multi-organ damage in animal studies. We previously reported the effect of GYY4137 on cardiac ischaemia reperfusion injury (IRI) in diabetic mice. However, the role and mechanism of GYY4137 in renal IRI are poorly understood. The aims of this study were to determine whether GYY4137 can effectively alleviate the injury induced by renal ischaemia reperfusion and to explore its possible mechanism. <b><i>Methods:</i></b> Mice received right nephrectomy and clipping of the left renal pedicle for 45 min. GYY4137 was administered by intraperitoneal injection for 2 consecutive days before the operation. The model of hypoxia/reoxygenation injury was established in HK-2 cells, which were pre-treated with or without GYY4137. Renal histology, function, apoptosis, and oxidative stress were measured. Western blot was used to measure the target ­protein after renal IRI. <b><i>Results:</i></b> The results indicated that GYY4137 had a clear protective effect on renal IRI as reflected by the attenuation of renal dysfunction, renal tubule injury, and apoptosis. Moreover, GYY4137 remarkably reduced renal IRI-induced oxidative stress. GYY4137 significantly elevated the nuclear translocation of nuclear factor-erythroid-2-related factor 2 (Nrf2) and the expression of antioxidant enzymes regulated by Nrf2, including SOD, HO-1, and NQO-1. <b><i>Conclusions:</i></b> GYY4137 alleviates ischaemia reperfusion-induced renal injury through activating the antioxidant effect mediated by Nrf2 signalling.

Exhaustive endurance exercise activates brain glycogen breakdown and lactate production more than insulin-induced hypoglycemia

2021 ◽  
Author(s):  
Takashi Matsui
Keyword(s):  
Endurance Exercise ◽  
Lactate Production ◽  
Severe Hypoglycemia ◽  
Exercise Group ◽  
Exhaustive Exercise ◽  
Endurance Capacity ◽  
Brain Glycogen ◽  
Insulin Group ◽  
Exercise Induced

Brain glycogen localized in astrocytes produces lactate via cAMP signaling, which regulates memory functions and endurance capacity. Exhaustive endurance exercise with hypoglycemia decreases brain glycogen, although the mechanism underlying this phenomenon remains unclear. Since insulin-induced hypoglycemia decreases brain glycogen, this study tested the hypothesis that hypoglycemia mediates exercise-induced brain glycogen decrease. To test the hypothesis, the effects of insulin- and exhaustive exercise-induced hypoglycemia on brain glycogen levels were compared using the microwave irradiation method in adult Wistar rats. The insulin challenge and exhaustive exercise induced similar levels of severe hypoglycemia. Glycogen in the hypothalamus and cerebellum decreased similarly with the insulin challenge and exhaustive exercise; however, glycogen in the cortex, hippocampus, and brainstem of the exercise group were lower compared to the insulin group. Blood glucose correlated positively with brain glycogen, but the slope of regression lines was greater in the exercise group compared to the insulin group in the cortex, hippocampus, and brainstem, but not the hypothalamus and cerebellum. Brain lactate and cAMP levels in the hypothalamus and cerebellum increased similarly with the insulin challenge and exhaustive exercise, but those in the cortex, hippocampus, and brainstem of the exercise group were higher compared to the insulin group. These findings support the hypothesis that hypoglycemia mediates the exercise-induced reduction in brain glycogen, at least in the hypothalamus and cerebellum. However, glycogen reduction during exhaustive endurance exercise in the cortex, hippocampus, and brainstem is not due to hypoglycemia alone, implicating the role of exercise-specific neuronal activity in brain glycogen decrease.

scholarly journals SOD Derived from Bacillus amyloliquefaciens GF423 Has Protection Against Exercise-Induced Oxidative Stress in Healthy Subjects

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 764-764
Author(s):  
Yea-eun Nam ◽  
Yunsoo Kim ◽  
Yeni Lim ◽  
Hye Jin Kim ◽  
Oran Kwon
Keyword(s):  
Oxidative Stress ◽  
Healthy Subjects ◽  
Antioxidant Defense ◽  
Maximal Oxygen Consumption ◽  
Intervention Group ◽  
Lipid Peroxides ◽  
Experimental Period ◽  
Cellular Damage ◽  
Double Blind ◽  
Exercise Induced

Abstract Objectives Excessive reactive oxygen species (ROS) can cause cellular damage, causing a variety of degenerative diseases such as atherosclerosis, ischemic heart disease, and cancer. SOD is thought to play a central role in scavenging ROS generated in cells by enhancing the antioxidant defense system, including catalase and glutathione peroxidase. This study aims to test the hypothesis that exogenous SOD administration can help to protect against oxidative stress encountered at very early stages in the daily life of healthy subjects. Methods A total of 80 healthy adults were assigned to either an intervention group consuming B. amyloliquefaciens GF423 SOD (250 IU/capsule) daily for 8 weeks or a placebo in a randomized, double-blind and parallel design. Aerobic exercise by a treadmill for 30 minutes at an intensity of 60% of the maximal oxygen consumption (VO2max) of each subject was used to induce oxidative stress at the beginning and end of the experimental period. Blood and urine samples were collected immediately after and 30 min after the exercise challenge to measure biochemical markers related to oxidative stress and inflammation. Results A single administration of exogenous SOD induced a marked decrease in urinary lipid peroxides and plasma pro-inflammatory cytokines as compared to placebo administration. Furthermore, repeated administration of exogenous SOD for eight weeks resulted in a significant improvement of erythrocyte redox balance. Conclusions These findings suggest that the supply of exogenous SOD may be useful to enhance the antioxidant defense capacity and anti-inflammatory response in response to exercise-induced oxidative stress. Funding Sources This work was supported by the Bio-Synergy Research Project (NRF-2012M3A9C4048761) from the Ministry of Science, ICT, and Future Planning, and the BK21PLUS (Brain Korea 21 plus) program (22a20130012143) from the Ministry of Education and the GenoFocus Inc, Republic of Korea.

scholarly journals Oxidative stress and genetic markers of suboptimal antioxidant defense in the aging brain: a theoretical review

2014 ◽  
Vol 25 (6) ◽  
Author(s):  
Lauren E. Salminen ◽  
Robert H. Paul
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Defense ◽  
Future Research ◽  
Aging Brain ◽  
Older Individuals ◽  
Glutathione S Transferase ◽  
Antioxidant Defense Enzymes ◽  
Repair Mechanisms ◽  
The Impact ◽  
The Brain

AbstractNormal aging involves a gradual breakdown of physiological processes that leads to a decline in cognitive functions and brain integrity, yet the onset and progression of decline are variable among older individuals. While many biological changes may contribute to this degree of variability, oxidative stress is a key mechanism of the aging process that can cause direct damage to cellular architecture within the brain. Oligodendrocytes are at a high risk for oxidative damage due to their role in myelin maintenance and production and limited repair mechanisms, suggesting that white matter may be particularly vulnerable to oxidative activity. Antioxidant defense enzymes within the brain, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione-S-transferase (GST), are crucial for breaking down the harmful end products of oxidative phosphorylation. Previous studies have revealed that allele variations of polymorphisms that encode these antioxidants are associated with abnormalities in SOD, CAT, GPx, and GST activity in the central nervous system. This review will focus on the role of oxidative stress in the aging brain and the impact of decreased antioxidant defense on brain integrity and cognitive function. Directions for future research investigations of antioxidant defense genes will also be discussed.

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