Exercise-Induced Oxidative DNA Damage and Lymphocytopenia in Sedentary Young Males

Tanimura, Yuko; Shimizu, Kazuhiro; Tanabe, Kai; Otsuki, Takeshi; Yamauchi, Ryohei; Matsubara, Y; Iemitsu, Motoyuki; Maeda, Seiji; Ajisaka, Ryuichi

doi:10.1249/mss.0b013e31817242cf

Cited by 30 publications

(21 citation statements)

References 40 publications

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“…•-has been reported to be increased in the brain (Pedreanez et al, 2006), skeletal muscle (Brooks et al, 2008), peritoneal macrophages (De la Fuente et al, 1995), neutrophils (Garcia et al, 2011) and lymphocytes (Tanimura et al, 2008). Similarly, • NO has been reported to be increased in skeletal muscle (Brooks et al, 2008), CD34…”

Section: Multiple Sources and Tissues Generate Reactive Species Durinmentioning

confidence: 98%

Redox biology of exercise: an integrative and comparative consideration of some overlooked issues

Nikolaidis

Kyparos

Spanou

et al. 2012

Journal of Experimental Biology

124

152

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SummaryThe central aim of this review is to address the highly multidisciplinary topic of redox biology as related to exercise using an integrative and comparative approach rather than focusing on blood, skeletal muscle or humans. An attempt is also made to redefine ʻoxidative stressʼ as well as to introduce the term ʻalterations in redox homeostasisʼ to describe changes in redox homeostasis indicating oxidative stress, reductive stress or both. The literature analysis shows that the effects of non-muscledamaging exercise and muscle-damaging exercise on redox homeostasis are completely different. Non-muscle-damaging exercise induces alterations in redox homeostasis that last a few hours post exercise, whereas muscle-damaging exercise causes alterations in redox homeostasis that may persist for and/or appear several days post exercise. Both exhaustive maximal exercise lasting only 30s and isometric exercise lasting 1-3min (the latter activating in addition a small muscle mass) induce systemic oxidative stress. With the necessary modifications, exercise is capable of inducing redox homeostasis alterations in all fluids, cells, tissues and organs studied so far, irrespective of strains and species. More importantly, ʻexercise-induced oxidative stressʼ is not an ʻoddityʼ associated with a particular type of exercise, tissue or species. Rather, oxidative stress constitutes a ubiquitous fundamental biological response to the alteration of redox homeostasis imposed by exercise. The hormesis concept could provide an interpretative framework to reconcile differences that emerge among studies in the field of exercise redox biology. Integrative and comparative approaches can help determine the interactions of key redox responses at multiple levels of biological organization.Key words: antioxidant, biomarker, eccentric, free radical, training. THE JOURNAL OF EXPERIMENTAL BIOLOGY 1616The ʻgoodʼ (antioxidants), the ʻbadʼ (reactive species) and the ʻuglyʼ (oxidative stress) 1 The distinction drawn in the section heading is schematically used to parody the popular manichaeistic view that antioxidants are considered 'useful' entities, reactive species are considered 'harmful' entities and oxidative stress is considered a 'negative' state. Certainly, the reality is much more complicated and antioxidants, reactive species and oxidative stress can serve both useful and detrimental roles, which are dependent on the biological context (within an organism), which in turn are greatly dependent on the environmental context (outside an organism). AntioxidantsAdmittedly, to define the term 'antioxidant' is a difficult task. In this paper, antioxidant is defined as any mechanism, structure and/or substance that delays, prevents or removes oxidative modifications to a target molecule (Halliwell and Gutteridge, 2007;Pamplona and Costantini, 2011). Antioxidants can be complex molecules such as the superoxide dismutases and peroxiredoxins, or simpler ones such as uric acid and glutathione (Gutteridge and Halliwell, 2010). They can be broa...

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Section: Multiple Sources and Tissues Generate Reactive Species Durinmentioning

confidence: 98%

Redox biology of exercise: an integrative and comparative consideration of some overlooked issues

Nikolaidis

Kyparos

Spanou

et al. 2012

Journal of Experimental Biology

124

152

View full text Add to dashboard Cite

show abstract

“…Numerous human studies have reported the physiological eVects of the two types of exercise. Acute exercise-induced generation of reactive oxygen species (ROS) contributes to acute exercise-induced lymphocyte apoptosis and has a negative impact on post-exercise immune suppression (Mooren et al 2002;Tanimura et al 2008;Tsai et al 2001). However, regular physical activity is generally considered to enhance antioxidant capacity and improve cardiac function and can prevent the prevalence of type 2 diabetes mellitus in humans (GomezCabrera et al 2008; Thompson et al 2007;Gill and Cooper 2008).…”

Section: Introductionmentioning

confidence: 99%

Metabolomics investigation of exercise-modulated changes in metabolism in rat liver after exhaustive and endurance exercises

et al. 2009

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Exhaustive exercise and endurance exercise training modify the physiological status of the body differently. The present study aimed to evaluate the alteration in biochemical composition with exhaustive and endurance exercises in rats using metabolomics strategy. The metabolite profile of liver tissue was investigated on gas chromatography-mass spectrometry (GC-MS). Data further underwent partial least-squares-discriminant analysis (PLS-DA) to compare the effects on metabolites in sedentary control, exhaustively exercised and endurance trained rats. GC-MS detected 115 highly reproducible peaks in chromatograms from individual liver tissue extracts, and we identified 55 of them. The three groups showed significant differences in metabolic profile. Changes in liver metabolism involved metabolites such as amino acids, fatty acids, organic acids, and carbohydrates. Endurance training elevated the greater rate of tricarboxylic acid cycle and antioxidant activity, and exhaustive exercise led to accumulated urea markers and an inflammation response in liver. In addition, GC-MS-based metabolomic analysis is a promising tool to investigate a pathological status with different exercise programs.

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“…Numerous human studies suggest that acute exercise-induced generation of reactive oxygen species (ROS) contributes to acute exercise-induced lymphocyte apoptosis and has a negative impact on post-exercise immune suppression (Mooren et al 2002;Tanimura et al 2008;Tsai et al 2001). Exhaustive exercise induces free radicals in vivo and leads to oxidative damage in the heart of young and aging rats (Frankiewicz-Jósko et al 1996;Huang et al 2008;Kim and Chi 1997).…”

Section: Introductionmentioning

confidence: 99%

Endurance training accelerates exhaustive exercise-induced mitochondrial DNA deletion and apoptosis of left ventricle myocardium in rats

et al. 2009

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Even though exhaustive exercise-induced oxidative stress increases the risk of tissue damage, regular endurance training is widely assumed to improve cardiac function and protects against heart disease. We tested the hypothesis that an endurance training program prevents exhaustive exercise-induced increases in cardiac dysfunction and apoptosis in left ventricle (LV). Thirty-two male Sprague-Dawley rats were randomly divided into four groups: sedentary control (C), trained (T), exhaustively exercised (E), and trained plus exhaustively exercised (TE). Rats in T and TE groups ran on a motorized treadmill for 12 weeks. Rats in groups E and TE performed an exhaustive running test on a treadmill. The main effects of training were indicated by increased running time to exhaustion (80 +/- 5 and 151 +/- 13 min for groups E and TE, respectively, P = 0.0001), myocardial hypertrophy (0.38% and 0.47% for untrained and trained rats, respectively, P = 0.0002), decreased LV ejection fraction (88% and 71% for untrained and trained rats, respectively, P < 0.0001), accelerated mitochondrial DNA 4834-bp large deletion (mtDNA4834 deletion), and up-regulated protein levels of heat shock protein-70, cytochrome C, cleaved capsase-3, and cleaved PARP in LV following a bout of exhaustive exercise. Contrary to our hypothesis, these results suggest that endurance training induced significant impairment of regional systolic and diastolic LV myocardial function and ejection fraction in rats. Our findings show that endurance training accelerates exhaustive exercise-induced mtDNA4834 deletion and apoptosis in the LV.

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Exercise-Induced Oxidative DNA Damage and Lymphocytopenia in Sedentary Young Males

Abstract: Results of this study suggest that lymphocyte oxidative DNA damage can relate to lymphocytopenia, although DNA damage was not associated with apoptosis in healthy young sedentary males.

Cited by 30 publications

References 40 publications

Redox biology of exercise: an integrative and comparative consideration of some overlooked issues

Redox biology of exercise: an integrative and comparative consideration of some overlooked issues

Metabolomics investigation of exercise-modulated changes in metabolism in rat liver after exhaustive and endurance exercises

Endurance training accelerates exhaustive exercise-induced mitochondrial DNA deletion and apoptosis of left ventricle myocardium in rats

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