Sulforaphane treatment protects skeletal muscle against damage induced by exhaustive exercise in rats.
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.
Malaguti
Marco
M
Dipartimento di Biochimica G. Moruzzi, Alma Mater Studiorum-Università di Bologna, Via Irnerio, 48, Bologna 40126, Italy.
Angeloni
Cristina
C
Garatachea
Nuria
N
Baldini
Marta
M
Leoncini
Emanuela
E
Collado
Pilar S
PS
Teti
Gabriella
G
Falconi
Mirella
M
Gonzalez-Gallego
Javier
J
Hrelia
Silvana
S
D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D003402:Creatine Kinase / Q000097:blood; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D017879:Isothiocyanates; D007770:L-Lactate Dehydrogenase / Q000097:blood; D008297:Male; D009135:Muscular Diseases / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D016660:NAD(P)H Dehydrogenase (Quinone) / Q000378:metabolism; D051267:NF-E2-Related Factor 2 / Q000378:metabolism; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000187:drug effects*; D005082:Physical Exertion; D052097:Quadriceps Muscle / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D013454:Sulfoxides; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D013861:Thiocyanates / Q000494:pharmacology*; D013880:Thioredoxin-Disulfide Reductase / Q000378:metabolism
D000975:Antioxidants; D017879:Isothiocyanates; D051267:NF-E2-Related Factor 2; C495637:Nfe2l2 protein, rat; D013454:Sulfoxides; D017392:Thiobarbituric Acid Reactive Substances; D013861:Thiocyanates; D007770:L-Lactate Dehydrogenase; D005979:Glutathione Peroxidase; D016660:NAD(P)H Dehydrogenase (Quinone); C507703:NQO1 protein, rat; D005980:Glutathione Reductase; D013880:Thioredoxin-Disulfide Reductase; D005982:Glutathione Transferase; D003402:Creatine Kinase; C016766:sulforaphane