Antioxidant supplementation influences the neutrophil tocopherol associated protein expression, but not the inflammatory response to exercise

2007 ◽  
Vol 2 (1) ◽  
pp. 56-70 ◽  
Author(s):  
Antoni Sureda ◽  
Pedro Tauler ◽  
Antoni Aguiló ◽  
Nuria Cases ◽  
Isabel Llompart ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Placebo Group ◽  
Inflammatory Response ◽  
Exhaustive Exercise ◽  
Plasma Damage ◽  
Marathon Race ◽  
Neutrophil Degranulation ◽  
Exercise Induced ◽  
Antioxidant Diet ◽  
Diet Supplementation

AbstractIntense exercise induces inflammatory-like changes and oxidative stress in immune cells. Our aim was to study the effects of antioxidant diet supplementation on the neutrophil inflammatory response and on the tocopherol associated protein (TAP) expression after exhaustive exercise. Fourteen male-trained amateur runners were randomly divided in two placebo and supplemented groups. Vitamins C (152 mg/d) and E (50 mg/d) supplementation were administrated to the athletes for a month, using an almond based isotonic and energetic beverage. Non-enriched beverage was given to the placebo group. After one month, the subjects participated in a half-marathon race (21 km-run). Neutrophil TAP mRNA expression and markers of the inflammatory response were determined before, immediately after, and 3 h after finishing the half-marathon race. TAP expression increased after exercise mainly in the neutrophils of the placebo group. Exercise induced an inflammatory response in both placebo and supplemented groups, manifested with neutrophilia, increased creatine kinase and lactate dehydrogenase serum activities, neutrophil luminol chemiluminescence and myeloperoxidase release. Plasma malondialdehyde only increased in the placebo group after exercise. Diet supplementation with moderate levels of antioxidant vitamins avoids plasma damage in response to exhaustive exercise without the effects on the inflammatory process. Neutrophil degranulation and increased tocopherol associated protein could contribute to the neutrophil protection from the oxidative stress.

Protective role of l-carnitine supplementation against exhaustive exercise induced oxidative stress in rats

2011 ◽  
Vol 668 (3) ◽  
pp. 407-413 ◽  
Author(s):  
Elif Şıktar ◽  
Deniz Ekinci ◽  
Erdinç Şıktar ◽  
Şükrü Beydemir ◽  
İlhami Gülçin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protective Role ◽  
Exhaustive Exercise ◽  
Carnitine Supplementation ◽  
Exercise Induced

scholarly journals P604Cardiac effects of exhaustive exercise induced oxidative stress in a rat model

2014 ◽  
Vol 103 (suppl 1) ◽  
pp. S109.2-S109
Author(s):  
A Olah ◽  
BT Nemeth ◽  
C Matyas ◽  
L Hidi ◽  
E Birtalan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Rat Model ◽  
Exhaustive Exercise ◽  
Exercise Induced

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.

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 Acute Exercise-Induced Mitochondrial Stress Triggers an Inflammatory Response in the Myocardium via NLRP3 Inflammasome Activation with Mitophagy

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Haiying Li ◽  
Weiguo Miao ◽  
Jingfen Ma ◽  
Zhen Xv ◽  
Hai Bo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Nlrp3 Inflammasome ◽  
Acute Exercise ◽  
Inflammasome Activation ◽  
Heavy Exercise ◽  
Mitochondrial Stress ◽  
Nlrp3 Inflammasome Activation ◽  
Exercise Induced ◽  
Related Proteins

Increasing evidence has indicated that acute strenuous exercise can induce a range of adverse reactions including oxidative stress and tissue inflammation. However, little is currently known regarding the mechanisms that underlie the regulation of the inflammatory response in the myocardium during acute heavy exercise. This study evaluated the mitochondrial function, NLRP3 inflammasome activation, and mitochondrial autophagy-related proteins to investigate the regulation and mechanism of mitochondrial stress regarding the inflammatory response of the rat myocardium during acute heavy exercise. The results indicated that the mitochondrial function of the myocardium was adaptively regulated to meet the challenge of stress during acute exercise. The exercise-induced mitochondrial stress also enhanced ROS generation and triggered an inflammatory reaction via the NLRP3 inflammasome activation. Moreover, the mitochondrial autophagy-related proteins including Beclin1, LC3, and Bnip3 were all significantly upregulated during acute exercise, which suggests that mitophagy was stimulated in response to the oxidative stress and inflammatory response in the myocardium. Taken together, our data suggest that, during acute exercise, mitochondrial stress triggers the rat myocardial inflammatory response via NLRP3 inflammasome activation and activates mitophagy to minimize myocardial injury.

scholarly journals Effects of CoQ10 supplementation and swimming training on exhaustive exercise-induced oxidative stress in rat heart

2012 ◽  
Vol 113 (07) ◽  
pp. 393-399 ◽  
Author(s):  
N. Okudan ◽  
S. Revan ◽  
S. S. Balci ◽  
M. Belviranli ◽  
H. Pepe ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Rat Heart ◽  
Exhaustive Exercise ◽  
Swimming Training ◽  
Coq10 Supplementation ◽  
Exercise Induced
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