Document Detail


Sulforaphane treatment protects skeletal muscle against damage induced by exhaustive exercise in rats.
MedLine Citation:
PMID:  19713431     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Sulforaphane (SF), one of the most important isothiocyanates in the human diet, present in cruciferous vegetables, is known to have chemopreventive activities in different tissues. No data are available on its effects in the prevention of skeletal muscle damage. In this study, we investigated the potential protective effects of SF treatment on muscle damage and oxidative stress induced by an acute bout of exhaustive exercise in rats. Male Wistar rats were treated with SF (25 mg/kg body wt ip) for 3 days before undergoing an acute exhaustive exercise protocol in a treadmill (+7% slope and 24 m/min). Acute exercise resulted in a significant increase in plasma lactate dehydrogenase (LDH) and creatine phosphokinase (CPK) activities. It also resulted in a significant increase in thiobarbituric acid-reactive substances, in a significant decrease in tissue total antioxidant capacity, and in a significant decrease in NAD(P)H:quinone oxidoreductase 1 (NQO1) expression and activity in vastus lateralis muscle. SF treatment significantly increased muscle NQO1, glutathione-S-transferase, and glutathione reductase expression and activity, with no effect on glutathione peroxidase and thioredoxin reductase. The observed SF-induced upregulation of phase II enzymes was accompanied by a significant increase in nuclear erythroid 2 p45-related factor 2 expression and correlated with a significant increase in total antioxidant capacity and a decrease in plasma LDH and CPK activities. Our data demonstrate that SF acts as an indirect antioxidant in skeletal muscle and could play a critical role in the modulation of the muscle redox environment, leading to the prevention of exhaustive exercise-induced muscle damage.
Authors:
Marco Malaguti; Cristina Angeloni; Nuria Garatachea; Marta Baldini; Emanuela Leoncini; Pilar S Collado; Gabriella Teti; Mirella Falconi; Javier Gonzalez-Gallego; Silvana Hrelia
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-08-27
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  107     ISSN:  1522-1601     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2009 Oct 
Date Detail:
Created Date:  2009-10-16     Completed Date:  2009-12-24     Revised Date:  2013-09-26    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1028-36     Citation Subset:  IM    
Affiliation:
Dipartimento di Biochimica G. Moruzzi, Alma Mater Studiorum-Università di Bologna, Via Irnerio, 48, Bologna 40126, Italy.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antioxidants / pharmacology*
Creatine Kinase / blood
Glutathione Peroxidase / metabolism
Glutathione Reductase / metabolism
Glutathione Transferase / metabolism
L-Lactate Dehydrogenase / blood
Male
Muscular Diseases / metabolism,  pathology,  prevention & control*
NAD(P)H Dehydrogenase (Quinone) / metabolism
NF-E2-Related Factor 2 / metabolism
Oxidation-Reduction
Oxidative Stress / drug effects*
Physical Exertion*
Quadriceps Muscle / drug effects*,  metabolism,  pathology
Rats
Rats, Wistar
Thiobarbituric Acid Reactive Substances / metabolism
Thiocyanates / pharmacology*
Thioredoxin-Disulfide Reductase / metabolism
Chemical
Reg. No./Substance:
0/Antioxidants; 0/NF-E2-Related Factor 2; 0/Nfe2l2 protein, rat; 0/Thiobarbituric Acid Reactive Substances; 0/Thiocyanates; 4478-93-7/sulforafan; EC 1.1.1.27/L-Lactate Dehydrogenase; EC 1.11.1.9/Glutathione Peroxidase; EC 1.6.5.2/NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2/NQO1 protein, rat; EC 1.8.1.7/Glutathione Reductase; EC 1.8.1.9/Thioredoxin-Disulfide Reductase; EC 2.5.1.18/Glutathione Transferase; EC 2.7.3.2/Creatine Kinase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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