Supplementation with vitamin C and N-acetyl-cysteine increases oxidative stress in humans after an acute muscle injury induced by eccentric exercise

Childs, April C.; Jacobs, Chelsea; Kaminski, Thomas W.; Halliwell, Barry; Leeuwenburgh, Christiaan

doi:10.1016/s0891-5849(01)00640-2

Cited by 302 publications

(261 citation statements)

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“…By increasing the availability of catalytic iron, AA may Vitamin C, DNA damage and iron homeostasis 21 exacerbate the formation of hydroxyl radical in inflammatory states. This hypothesis is supported by a human supplementation study where AA augmented the levels of bleomycin-detectable iron in the serum and the levels of lipid hydroperoxide during induced acute inflammation [67]. Ultimately, AA may accelerate the iron-dependent, oxidative stress-mediated destruction of normal tissues, a deleterious consequence of inflammatory reactions commonly observed in rheumatoid arthritis and other chronic inflammatory conditions [68,69].…”

Section: Potential Role Of Aa In Oxidative Cell Injury In Vivomentioning

confidence: 86%

Vitamin C modulation of H2O2-induced damage and iron homeostasis in human cells

Duarte

Jones

2007

Free Radical Biology and Medicine

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Vitamin C (ascorbic acid, AA) is an important antioxidant in human plasma. It is clear, however, that AA has other important, non-antioxidant roles in cells. Of particular interest is its involvement in iron metabolism, since AA enhances dietary iron absorption, increases the activity of Fe 2+ -dependent cellular enzymes, promotes Fenton reactions in vitro and was reported to have deleterious effects in individuals with iron overload. Nevertheless, the ability of AA to modulate iron metabolism and enhance iron-dependent damage in cells, tissues and organisms has not been fully elucidated. Here we investigated the effect of AA on iron-mediated oxidative stress in normal human fibroblasts. Incubation with physiologically relevant concentrations of AA was not harmful but sensitised cells towards H 2 O 2 -induced, iron-dependent DNA strand breakage and cell death. We also report that AA increased the levels of intracellular catalytic iron and concomitantly modulated the expression of two wellestablished iron-regulated genes, ferritin and transferrin receptor. In summary, we present evidence of a novel, non-antioxidant role of AA in human cells, where it increases iron availability and enhances ROS-mediated, iron-dependent damage. We suggest that AA may exacerbate the deleterious effects of metals in vivo and promote normal tissue injury in situations associated with elevated ROS production.

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Section: Potential Role Of Aa In Oxidative Cell Injury In Vivomentioning

confidence: 86%

Vitamin C modulation of H2O2-induced damage and iron homeostasis in human cells

Duarte

Jones

2007

Free Radical Biology and Medicine

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“…Ascorbic acid and n-aceltyl-l-cysteine as well as other antioxidants have different reactivities for specific oxidative species, such as hydroxyl radicals, singlet oxygen, hydrogen peroxide, peroxyl radicals, or superoxide anion [10,11]. Understanding how each of these two compounds reacts with ATO may provide new insights into their potential influence on the clinical outcome of APL patients receiving ATO chemotherapy.…”

Section: Introductionmentioning

confidence: 99%

Differential effect of ascorbic acid and n‐acetyl‐l‐cysteine on arsenic trioxide‐mediated oxidative stress in human leukemia (HL‐60) Cells

Yedjou

Rogers

Brown

et al. 2008

J Biochem & Molecular Tox

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Arsenic trioxide (ATO) has been recommended for the treatment of refractory cases of acute promyelocytic leukemia (APL). Recent studies in our laboratory indicated that oxidative stress plays a key role in ATO-induced cytotoxicity in human leukemia (HL-60) cells. In the present investigation, we performed the MTT assay and trypan blue exclusion test for cell viability. We also performed the thiobarbituric acid test to determine the levels of malondialdehyde (MDA) production in HL-60 cells co-exposed to either ascorbic acid (AA) and ATO or to n-acetyl-l-cysteine (NAC) and ATO. The results of MTT assay indicated that AA exposure potentiates the cytotoxicity of ATO in HL-60 cells, as evidenced by a gradual increase in MDA levels with increasing doses of AA. In contrary, the addition of NAC to ATO-treated HL-60 cells resulted in a dose dependent decrease of MDA production. From these results, we conclude that the addition of the ascorbic acid to ATO-treated HL-60 cells enhances the formation of reactive oxygen species (ROS) whereas the addition of NAC under the same experimental condition significantly (p<0.05) decreases the level of ROS formation. Based on these direct in vitro findings, our studies provide evidence that AA may extend the therapeutic spectrum of ATO. The co-administration of NAC with ATO shows a potential specificity for tumor cells, indicating it may not enhance the clinical outcome associated with ATO monotherapy in vivo.

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“…Σημαντικός αριθμός από αυτές παρουσίασαν παρόμοιες συγκεντρώσεις υπεροξείδωσης λιπιδίων (Cannon, et al, 1990;Child, et al, 1999;Sacheck, Decker, & Clarkson, 2000;Sacheck, Milbury, Cannon, Roubenoff, & Blumberg, 2003;Saxton, Donnelly, & Roper, 1994;You, et al, 2005). Οι περισσότερες εργασίες ωστόσο, αναφέρουν σημαντικά υψηλότερες συγκεντρώσεις υπεροξείδωσης λιπιδίων (Childs, Jacobs, Kaminski, Halliwell, & Leeuwenburgh, 2001;Close, et al, 2006;Close, et al, 2004;Close, Ashton, Cable, et al, 2005;Maughan, et al, 1989;Nikolaidis, et al, 2007;Paschalis, et al, 2007;Paschalis, Nikolaidis, et al, 2010a) σε ένα τουλάχιστον χρονικό σημείο μετά την άσκηση. Σημαντικό στοιχείο που προέκυψε από αυτές τις εργασίες είναι ότι δεν είχε αναφερθεί καμία επίδραση της έκκεντρης άσκησης στην λιπιδική υπεροξείδωση τις πρώτες ώρες μετά το τέλος της άσκησης (Cannon, et al, 1990;Close, et al, 2004;Close, Ashton, Cable, et al, 2005c;Goldfarb, et al, 2005;Nikolaidis, et al, 2007;Paschalis, et al, 2007;Paschalis, Nikolaidis, et al, 2010a;Sacheck, et al, 2000;Sacheck, et al, 2003).…”

Section: έκκεντρη άσκηση και οξειδοαναγωγική κατάσταση του αίματοςunclassified

“…Στην συγκεκριμένη εργασία έγινε λήψη βιταμίνης C για 2 εβδομάδες πριν την άσκηση και 3 μέρες μετά την άσκηση, διάστημα όπου και έγιναν φυσιολογικές και βιοχημικές μετρήσεις δεικτών μυϊκής απόδοσης και βλάβης (Thompson, et al, 2001). μειονέκτημα της συγκεκριμένης εργασίας είναι ο μικρός αριθμός συμμετεχόντων (7 ανά ομάδα) και το γεγονός ότι δεν χρησιμοποιήθηκε πειραματικός σχεδιασμός διασταύρωσης (cross-over design), κάτι το οποίο θα μείωνε σε μεγάλο βαθμό τις αρχικές διάφορες που υπήρχαν μεταξύ των ομάδων και θα μπορούσαν να επηρεάσουν το αποτέλεσμα (Childs, et al, 2001). …”

Section: έκκεντρη άσκηση και οξειδοαναγωγική κατάσταση του αίματοςunclassified

“…Σε αντίθεση με αυτές τις εργασίες, υπάρχουν εργασίες οι οποίες αναφέρουν ακριβώς τις αντίθετες επιδράσεις της λήψης βιταμίνης C και Ε σε δείκτες μυϊκής απόδοσης και οξειδωτικού στρες (Childs, et al, 2001;Close, et al, 2006) ή αντίστοιχες εργασίες που δεν αναφέρουν καμία επίδραση (Cannon, et al, 1990;Connolly, et al, 2006;Petersen, et al, 2001;Thompson, et al, 2001). Στην ουσία για κάθε εργασία η οποία αναφέρει μια θετική επίδραση σε ένα δείκτη μυϊκής βλάβης ή οξειδωτικού στρες υπάρχει η αντίστοιχη εργασία η οποία για τον ίδιο ή για κάποιο σχετικό δείκτη θα αναφέρει το αντίθετο αποτέλεσμα ή θα αναφέρει ότι η χορήγηση των βιταμινών δεν είχε καμία επίδραση.…”

Section: Petersen Et Al 2001unclassified

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Η Επίδραση Της Έκκεντρης Προπόνησης Σε Δείκτες Μυϊκής Βλάβης Και Οξειδωτικού Στρες

Θεοδώρου¹

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Anastasios A. Theodorou : The effect of eccentric training on muscle damage and redox status indices (Under the supervision of Athanasios Jamurtas, Assistand Professor)Antioxidant supplementation is quite often among athletes in an attempt to counteract the increased production of free radicals during exercise and especially after exerciseinduced muscle damage (eccentric). Recently an increasing number of studies reported negative effects of antioxidant supplementation on the training and cellular adaptations to chronic exercise. The aim of the present study was to investigate the effects of vitamin C and E supplementation on muscle performance, blood and muscle redox status, hemolysis and blood lipid profile in both trained and untrained individuals after acute and chronic exercise. After previous investigations of our group, a specific type of exercise was applied (eccentric) in order to produce long lasting and extensive changes in all biomarkers and examine more easily any effects of antioxidant supplementation. In a double-blinded fashion, participants received either a daily oral supplementation of vitamin C and vitamin E (n=14) or placebo (n=14) for eleven weeks. Following baseline tests, volunteers performed an eccentric exercise session two times per week for four weeks. Before and after the chronic eccentric exercise volunteers were subjected to one session of acute eccentric exercise, and physiological measurements were performed as well as blood samples and muscle biopsies (from 8 participants) were collected. The present results failed to support any effect of antioxidant supplementation; eccentric exercise similarly modified muscle damage and performance, blood redox status, hemolysis and lipid profile in both supplemented and non-supplemented groups. This is despite the fact that eccentric exercise induced marked changes in muscle damage and performance as well as redox status and lipid profile for several days after exercise. The complete lack of any effect on the physiological and biochemical outcome measures employed questions the validity of using orally antioxidant supplementation as redox modulators of muscle and redox status in healthy humans. Moreover, the lack of any effect of antioxidant supplementation on training and cellural adaptation to exercise observed in this study, opposed previous studies suggesting that antioxidant may block training adaptations.

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Supplementation with vitamin C and N-acetyl-cysteine increases oxidative stress in humans after an acute muscle injury induced by eccentric exercise

Cited by 302 publications

References 50 publications

Vitamin C modulation of H2O2-induced damage and iron homeostasis in human cells

Vitamin C modulation of H2O2-induced damage and iron homeostasis in human cells

Differential effect of ascorbic acid and n‐acetyl‐l‐cysteine on arsenic trioxide‐mediated oxidative stress in human leukemia (HL‐60) Cells

Η Επίδραση Της Έκκεντρης Προπόνησης Σε Δείκτες Μυϊκής Βλάβης Και Οξειδωτικού Στρες

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