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

被引:268
作者
Childs, A
Jacobs, C
Kaminski, T
Halliwell, B
Leeuwenburgh, C
机构
[1] Univ Florida, Coll Hlth & Human Performance, Ctr Exercise Sci, Biochem Aging Lab, Gainesville, FL 32611 USA
[2] Natl Univ Singapore, Dept Biochem, Singapore 117548, Singapore
关键词
pro-oxidants; ascorbic acid; neutrophils; sepsis; free radicals; disease; antioxidants;
D O I
10.1016/S0891-5849(01)00640-2
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
There has been no investigation to determine if the widely used over-the-counter, water-soluble antioxidants vitamin C and N-acetyl-cysteine (NAC) could act as pro-oxidants in humans during inflammatory conditions. We induced an acute-phase inflammatory response by an eccentric arm muscle injury. The inflammation was characterized by edema, swelling, pain, and increases in plasma inflammatory indicators, myeloperoxidase and interleukin-6. Immediately following the injury, subjects consumed a placebo or vitamin C (12.5 mg/kg body weight) and NAC (10 mg/kg body weight) for 7 d. The resulting muscle injury caused increased levels of serum bleomycin-detectable iron and the amount of iron was higher in the vitamin C and NAC group. The concentrations of lactate dehydrogenase (LDH), creatine kinase. (CK), and myoglobin were significantly elevated 2, 3, and 4 d postinjury and returned to baseline levels by day 7. In addition, LDH and CK activities were elevated to a greater extent in the vitamin C and NAC group. Levels of markers for oxidative stress (lipid hydroperoxides and 8-iso prostaglandin F-2 alpha; 8-Iso-PGF(2 alpha)) and antioxidant enzyme activities were also elevated post-injury. The subjects receiving vitamin C and NAC had higher levels of lipid hydroperoxides and 8-Iso-PGF(2 alpha) 2 d after the exercise. This acute human inflammatory model strongly suggests that vitamin C and NAC supplementation immediately post-injury, transiently increases tissue damage and oxidative stress. (C) 2001 Elsevier Science Inc.
引用
收藏
页码:745 / 753
页数:9
相关论文
共 59 条
  • [1] N-acetyl L-cysteine attenuates oxidant-mediated toxicity induced by chrysotile fibers
    Afaq, F
    Abidi, P
    Rahman, Q
    [J]. TOXICOLOGY LETTERS, 2000, 117 (1-2) : 53 - 60
  • [2] DIETARY CARCINOGENS AND ANTICARCINOGENS - OXYGEN RADICALS AND DEGENERATIVE DISEASES
    AMES, BN
    [J]. SCIENCE, 1983, 221 (4617) : 1256 - 1264
  • [3] BIOLOGICAL DEFENSE MECHANISMS - PRODUCTION BY LEUKOCYTES OF SUPEROXIDE A POTENTIAL BACTERICIDAL AGENT
    BABIOR, BM
    KIPNES, RS
    CURNUTTE, JT
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1973, 52 (03) : 741 - 744
  • [4] Heart, liver, and skeletal muscle myeloperoxidase activity during exercise
    Belcastro, AN
    Arthur, GD
    Albisser, TA
    Raj, DA
    [J]. JOURNAL OF APPLIED PHYSIOLOGY, 1996, 80 (04) : 1331 - 1335
  • [5] Antioxidant activity of vitamin C in iron-overloaded human plasma
    Berger, TM
    Polidori, MC
    Dabbagh, A
    Evans, PJ
    Halliwell, B
    Morrow, JD
    Roberts, LJ
    Frei, B
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (25) : 15656 - 15660
  • [6] IRON MOBILIZATION FROM FERRITIN BY SUPEROXIDE DERIVED FROM STIMULATED POLYMORPHONUCLEAR LEUKOCYTES - POSSIBLE MECHANISM IN INFLAMMATION DISEASES
    BIEMOND, P
    VANEIJK, HG
    SWAAK, AJG
    KOSTER, JF
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1984, 73 (06) : 1576 - 1579
  • [7] ON THE LIMITED ABILITY OF SUPEROXIDE TO RELEASE IRON FROM FERRITIN
    BOLANN, BJ
    ULVIK, RJ
    [J]. EUROPEAN JOURNAL OF BIOCHEMISTRY, 1990, 193 (03): : 899 - 904
  • [8] Interaction between 6-hydroxydopamine and transferrin: "Let my iron go''
    Borisenko, GG
    Kagan, VE
    Hsia, CJC
    Schor, NF
    [J]. BIOCHEMISTRY, 2000, 39 (12) : 3392 - 3400
  • [9] SUPEROXIDE ION AS A PRIMARY REDUCTANT IN ASCORBATE-MEDIATED FERRITIN IRON RELEASE
    BOYER, RF
    MCCLEARY, CJ
    [J]. FREE RADICAL BIOLOGY AND MEDICINE, 1987, 3 (06) : 389 - 395
  • [10] BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1016/0003-2697(76)90527-3