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dc.contributor.authorNikolaidis, Michalis G.
dc.contributor.authorJamurtas, Athanasios Z.
dc.contributor.authorPaschalis, Vassilis
dc.contributor.authorKostaropoulos, Iason A.
dc.contributor.authorKladi-Skandali, Athina
dc.contributor.authorBalamitsi, Vera
dc.contributor.authorKoutedakis, Yiannis
dc.contributor.authorKouretas, Dimitris
dc.date.accessioned2008-04-10T09:22:48Z
dc.date.available2008-04-10T09:22:48Z
dc.date.issued2006
dc.identifier.citationMedicine & Science in Sports & Exercise, 38(8): 1443-1450
dc.identifier.issn0195-9131
dc.identifier.pmid16888458
dc.identifier.doi10.1249/01.mss.0000228938.24658.5f
dc.identifier.urihttp://hdl.handle.net/2436/22857
dc.description.abstractPURPOSE: This study was designed to investigate whether individuals with glucose-6-phosphate dehydrogenase (G6PD) deficiency can exercise without greater perturbations in their redox status compared with non-G6PD-deficient individuals. METHODS: Nine males with established G6PD deficiency and nine males with normal G6PD activity performed two exhaustive treadmill exercise protocols of different duration (the shorter one lasting 12 min and the longer one 50 min). Several hematological parameters, reduced glutathione (GSH), oxidized glutathione (GSSG), thiobarbituric acid reactive substances (TBARS), protein carbonyls, catalase, and total antioxidant capacity (TAC) were measured in the blood before and after each exercise bout. RESULTS: Both GSH and GSSG were significantly higher in the control group compared with the G6PD-deficient group at baseline (0.404 +/- 0.101 vs 0.195 +/- 0.049 mmol.L(-1) for GSH and 0.047 +/- 0.012 vs 0.012 +/- 0.006 mmol.L(-1) for GSSG; P < 0.05); as a result, their ratio was not significantly different between the two groups (P > 0.05). All other oxidative stress indices were not different between groups at rest (P > 0.05). Exercise of both durations affected significantly (P < 0.05) and similarly the levels of all oxidative stress indices either in the G6PD-deficient group or in the control group. Only the long exercise affected GSH status significantly (P < 0.05), whereas both short and long exercise increased the levels of TBARS, protein carbonyls, catalase activity, and TAC to a similar extent (P < 0.05). CONCLUSION: G6PD-deficient individuals are able to exercise until exhaustion without higher oxidative stress compared with non-G6PD-deficient individuals. Exercise duration is an important determinant of the magnitude of exercise-induced changes for GSH, GSSG, and GSH/GSSG, but not for TBARS, protein carbonyls, catalase activity, or TAC.
dc.language.isoen
dc.publisherLippincott Williams & Wilkins
dc.relation.urlhttp://www.acsm-msse.org/pt/re/msse/abstract.00005768-200608000-00012.htm
dc.subject.meshAnalysis of Variance
dc.subject.meshAntioxidants
dc.subject.meshCatalase
dc.subject.meshExercise
dc.subject.meshExercise Test
dc.subject.meshGlucosephosphate Dehydrogenase Deficiency
dc.subject.meshGlutathione Disulfide
dc.subject.meshHumans
dc.subject.meshLipid Peroxidation
dc.subject.meshMale
dc.subject.meshOxidative Stress
dc.subject.meshProtein Carbonylation
dc.subject.meshStatistics, Nonparametric
dc.subject.meshThiobarbituric Acid Reactive Substances
dc.titleExercise-induced oxidative stress in G6PD-deficient individuals.
dc.typeJournal article
dc.identifier.journalMedicine & Science in Sports & Exercise
html.description.abstractPURPOSE: This study was designed to investigate whether individuals with glucose-6-phosphate dehydrogenase (G6PD) deficiency can exercise without greater perturbations in their redox status compared with non-G6PD-deficient individuals. METHODS: Nine males with established G6PD deficiency and nine males with normal G6PD activity performed two exhaustive treadmill exercise protocols of different duration (the shorter one lasting 12 min and the longer one 50 min). Several hematological parameters, reduced glutathione (GSH), oxidized glutathione (GSSG), thiobarbituric acid reactive substances (TBARS), protein carbonyls, catalase, and total antioxidant capacity (TAC) were measured in the blood before and after each exercise bout. RESULTS: Both GSH and GSSG were significantly higher in the control group compared with the G6PD-deficient group at baseline (0.404 +/- 0.101 vs 0.195 +/- 0.049 mmol.L(-1) for GSH and 0.047 +/- 0.012 vs 0.012 +/- 0.006 mmol.L(-1) for GSSG; P < 0.05); as a result, their ratio was not significantly different between the two groups (P > 0.05). All other oxidative stress indices were not different between groups at rest (P > 0.05). Exercise of both durations affected significantly (P < 0.05) and similarly the levels of all oxidative stress indices either in the G6PD-deficient group or in the control group. Only the long exercise affected GSH status significantly (P < 0.05), whereas both short and long exercise increased the levels of TBARS, protein carbonyls, catalase activity, and TAC to a similar extent (P < 0.05). CONCLUSION: G6PD-deficient individuals are able to exercise until exhaustion without higher oxidative stress compared with non-G6PD-deficient individuals. Exercise duration is an important determinant of the magnitude of exercise-induced changes for GSH, GSSG, and GSH/GSSG, but not for TBARS, protein carbonyls, catalase activity, or TAC.


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