title: Protective effects of L-arginine supplementation against exhaustive exercise-induced oxidative stress in young rat tissues.
abstract: Recently, we showed that L-arginine (L-Arg) supplementation could attenuate acute exercise-induced oxidative and inflammatory stress in aging rats. In this study, we investigate whether L-Arg supplementation protects cellular oxidative stress, inflammation, or the mitochondrial DNA 4834-bp large deletion (mtDNA4834 deletion) in 14-week-old young rats tissues during exhaustive exercise. Rats were randomly divided into four groups: sedentary control (SC); SC with L-Arg treatment (SC+Arg); exhaustive exercise (E); and exhaustive exercise with L-Arg treatment (E+Arg). Rats in the SC+Arg and E+Arg groups received supplemental 2% L-Arg diet. Rats in groups E and E+Arg performed an exhaustive running test on a treadmill. The results showed a significant increase in xanthine oxidase (XO) and myeloperoxidase (MPO) activities and lipid peroxide (malondialdehyde; MDA) levels of muscular, hepatic, and renal tissues in exercised rats as compared with sedentary rats. The increased XO, MPO, and MDA levels of these tissues significantly decreased in exercised rats supplemented with L-Arg. However, exhaustive exercise had no effect on mtDNA4834 deletions of muscular and hepatic tissues. The activities of creatine kinase (CK), aspartate aminotransferase (AST), alanine aminotransferase (ALT), blood urea nitrogen (BUN), creatinine (CRE), lactate, uric acid, non-esterified fatty acid (NEFA), and D-3-hydroxybutyrate in the plasma significantly increased in the exercised rats compared with the sedentary rats, while the CK, lactate and uric acid levels in the plasma significantly decreased in L-Arg-supplemented exercised rats. These findings suggest that L-Arg supplementation reduces the oxidative damage to and inflammatory response in skeletal muscles, the liver, and kidneys caused by exhaustive exercise in young rats.
authors.affiliation: Agricultural Biotechnology Research Center, Academia Sinica, Taipei 11529, Taiwan, ROC.
authors.forename: Chi-Chang
authors.initials: CC
authors.lastname: Huang
authors.forename: Tien-Jen
authors.initials: TJ
authors.lastname: Lin
authors.forename: Yi-Fa
authors.initials: YF
authors.lastname: Lu
authors.forename: Chun-Chieh
authors.initials: CC
authors.lastname: Chen
authors.forename: Chih-Yang
authors.initials: CY
authors.lastname: Huang
authors.forename: Wan-Teng
authors.initials: WT
authors.lastname: Lin
mesh_terms: D000818:Animals; D001120:Arginine / Q000008:administration & dosage / Q000494:pharmacology*; D003402:Creatine Kinase / Q000097:blood; D004272:DNA, Mitochondrial / Q000378:metabolism; D019587:Dietary Supplements; D005221:Fatigue / Q000503:physiopathology*; D007668:Kidney; D007773:Lactates / Q000097:blood; D008054:Lipid Peroxides / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D023421:Models, Animal; D018482:Muscle, Skeletal / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects* / Q000502:physiology*; D009195:Peroxidase / Q000378:metabolism; D010805:Physical Conditioning, Animal / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014527:Uric Acid / Q000097:blood; D014969:Xanthine Oxidase / Q000378:metabolism
chemical_list: D004272:DNA, Mitochondrial; D007773:Lactates; D008054:Lipid Peroxides; D014527:Uric Acid; D008315:Malondialdehyde; D001120:Arginine; D009195:Peroxidase; D014969:Xanthine Oxidase; D003402:Creatine Kinase