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Influence of vitamin C and vitamin E on redox signaling: Implications for exercise adaptations.
Free Radic Biol Med. 2015 Jul; 84:65-76.FR

Abstract

The exogenous antioxidants vitamin C (ascorbate) and vitamin E (α-tocopherol) often blunt favorable cell signaling responses to exercise, suggesting that redox signaling contributes to exercise adaptations. Current theories posit that this antioxidant paradigm interferes with redox signaling by attenuating exercise-induced reactive oxygen species (ROS) and reactive nitrogen species (RNS) generation. The well-documented in vitro antioxidant actions of ascorbate and α-tocopherol and characterization of the type and source of the ROS/RNS produced during exercise theoretically enable identification of redox-dependent mechanisms responsible for the blunting of favorable cell signaling responses to exercise. This review aimed to apply this reasoning to determine how the aforementioned antioxidants might attenuate exercise-induced ROS/RNS production. The principal outcomes of this analysis are (1) neither antioxidant is likely to attenuate nitric oxide signaling either directly (reaction with nitric oxide) or indirectly (reaction with derivatives, e.g., peroxynitrite); (2) neither antioxidant reacts appreciably with hydrogen peroxide, a key effector of redox signaling; (3) ascorbate but not α-tocopherol has the capacity to attenuate exercise-induced superoxide generation; and (4) alternate mechanisms, namely pro-oxidant side reactions and/or reduction of bioactive oxidized macromolecule adducts, are unlikely to interfere with exercise-induced redox signaling. Out of all the possibilities considered, ascorbate-mediated suppression of superoxide generation with attendant implications for hydrogen peroxide signaling is arguably the most cogent explanation for blunting of favorable cell signaling responses to exercise. However, this mechanism is dependent on ascorbate accumulating at sites rich in NADPH oxidases, principal contributors to contraction-mediated superoxide generation, and outcompeting nitric oxide and superoxide dismutase isoforms. The major conclusions of this review are: (1) direct evidence for interference of ascorbate and α-tocopherol with exercise-induced ROS/RNS production is lacking; (2) theoretical analysis reveals that both antioxidants are unlikely to have a major impact on exercise-induced redox signaling; and (3) it is worth considering alternate redox-independent mechanisms.

Authors+Show Affiliations

Division of Sport and Exercise Sciences, Abertay University, Dundee, UK, DD1 1HG. Electronic address: J.Cobley@abertay.ac.uk.Division of Sport and Exercise Sciences, Abertay University, Dundee, UK, DD1 1HG.Research Institute for Sport and Eqxercise Science, Liverpool John Moores University, Liverpool, UK, L3 3AF.School of Physical Education and Sport Sciences at Serres, Aristotle University of Thessaloniki, Serres, Greece.Research Institute for Sport and Eqxercise Science, Liverpool John Moores University, Liverpool, UK, L3 3AF.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

25841784

Citation

Cobley, James N., et al. "Influence of Vitamin C and Vitamin E On Redox Signaling: Implications for Exercise Adaptations." Free Radical Biology & Medicine, vol. 84, 2015, pp. 65-76.
Cobley JN, McHardy H, Morton JP, et al. Influence of vitamin C and vitamin E on redox signaling: Implications for exercise adaptations. Free Radic Biol Med. 2015;84:65-76.
Cobley, J. N., McHardy, H., Morton, J. P., Nikolaidis, M. G., & Close, G. L. (2015). Influence of vitamin C and vitamin E on redox signaling: Implications for exercise adaptations. Free Radical Biology & Medicine, 84, 65-76. https://doi.org/10.1016/j.freeradbiomed.2015.03.018
Cobley JN, et al. Influence of Vitamin C and Vitamin E On Redox Signaling: Implications for Exercise Adaptations. Free Radic Biol Med. 2015;84:65-76. PubMed PMID: 25841784.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Influence of vitamin C and vitamin E on redox signaling: Implications for exercise adaptations. AU - Cobley,James N, AU - McHardy,Helen, AU - Morton,James P, AU - Nikolaidis,Michalis G, AU - Close,Graeme L, Y1 - 2015/04/02/ PY - 2014/12/08/received PY - 2015/03/06/revised PY - 2015/03/06/accepted PY - 2015/4/6/entrez PY - 2015/4/7/pubmed PY - 2016/3/5/medline KW - Antioxidant KW - Exercise adaptations KW - Oxidative stress KW - Reactive nitrogen species KW - Reactive oxygen species KW - Vitamin C KW - Vitamin E SP - 65 EP - 76 JF - Free radical biology & medicine JO - Free Radic. Biol. Med. VL - 84 N2 - The exogenous antioxidants vitamin C (ascorbate) and vitamin E (α-tocopherol) often blunt favorable cell signaling responses to exercise, suggesting that redox signaling contributes to exercise adaptations. Current theories posit that this antioxidant paradigm interferes with redox signaling by attenuating exercise-induced reactive oxygen species (ROS) and reactive nitrogen species (RNS) generation. The well-documented in vitro antioxidant actions of ascorbate and α-tocopherol and characterization of the type and source of the ROS/RNS produced during exercise theoretically enable identification of redox-dependent mechanisms responsible for the blunting of favorable cell signaling responses to exercise. This review aimed to apply this reasoning to determine how the aforementioned antioxidants might attenuate exercise-induced ROS/RNS production. The principal outcomes of this analysis are (1) neither antioxidant is likely to attenuate nitric oxide signaling either directly (reaction with nitric oxide) or indirectly (reaction with derivatives, e.g., peroxynitrite); (2) neither antioxidant reacts appreciably with hydrogen peroxide, a key effector of redox signaling; (3) ascorbate but not α-tocopherol has the capacity to attenuate exercise-induced superoxide generation; and (4) alternate mechanisms, namely pro-oxidant side reactions and/or reduction of bioactive oxidized macromolecule adducts, are unlikely to interfere with exercise-induced redox signaling. Out of all the possibilities considered, ascorbate-mediated suppression of superoxide generation with attendant implications for hydrogen peroxide signaling is arguably the most cogent explanation for blunting of favorable cell signaling responses to exercise. However, this mechanism is dependent on ascorbate accumulating at sites rich in NADPH oxidases, principal contributors to contraction-mediated superoxide generation, and outcompeting nitric oxide and superoxide dismutase isoforms. The major conclusions of this review are: (1) direct evidence for interference of ascorbate and α-tocopherol with exercise-induced ROS/RNS production is lacking; (2) theoretical analysis reveals that both antioxidants are unlikely to have a major impact on exercise-induced redox signaling; and (3) it is worth considering alternate redox-independent mechanisms. SN - 1873-4596 UR - https://www.unboundmedicine.com/medline/citation/25841784/Influence_of_vitamin_C_and_vitamin_E_on_redox_signaling:_Implications_for_exercise_adaptations_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0891-5849(15)00142-2 DB - PRIME DP - Unbound Medicine ER -