title: Oxidant production and immune response after stretch injury in skeletal muscle.
abstract: OBJECTIVE
  This study investigated oxidant production and associated immune response after acute muscle stretch injury.
  
  
  METHODS
  A standardized single stretch injury was performed on the tibialis anterior (TA) muscle of 36 male New Zealand white rabbits while contralateral control limbs underwent a sham surgery. Animals were sacrificed 0, 4, 12, 24, 48, and 72 h after injury. Potential sites of oxidant production, measured with a dichlorofluorescein (DCF) probe, were evaluated using two separate buffers.
  
  
  RESULTS
  Nonmitochondrial oxidant production measured under basal buffer conditions (0.1 M potassium phosphate) was increased in both injured and control limbs at 24 h (P < 0.01) and was greater in the injured limb at 12 and 48 h (P < 0.01). There was also an interaction of time and injury (P < 0.05). Maximum oxidant production by neutrophils and macrophages, stimulated by the induced buffer (including 1.7 mM ADP, 0.1 mM NADPH, 0.1 mM FeCl3), was increased in both injured and control limbs at 4 h (P < 0.01) and was greater in the injured limb at 48 h (P < 0.01). Myeloperoxidase (MPO) activity, indicating the presence of activated neutrophils, was higher in the injured limb at 4 and 48 h (P < 0.01). The activities of superoxide radical producing and quenching enzymes, xanthine oxidase (XO) and superoxide dismutase (SOD), were elevated at 24 (P < 0.01) and 4 h (P < 0.05), respectively, but showed no difference between injured and control limbs.
  
  
  CONCLUSIONS
  We conclude that acute muscle stretch injury and the required surgeries to generate the injury result in a biphasic increase in oxidant production in both injured and control limbs, suggesting a systemic immune response. The increase in oxidant production at 4 h may be caused by an increase in activated neutrophils, whereas XO activity may contribute to oxidant generation at 24 h.
authors.affiliation: Department of Family Medicine, University of Wisconsin Medical School, 621 Science Drive, Madison, WI 53711, USA.
authors.forename: S
authors.initials: S
authors.lastname: Brickson
authors.forename: J
authors.initials: J
authors.lastname: Hollander
authors.forename: D T
authors.initials: DT
authors.lastname: Corr
authors.forename: L L
authors.initials: LL
authors.lastname: Ji
authors.forename: T M
authors.initials: TM
authors.lastname: Best
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D007869:Leg Injuries / Q000378:metabolism*; D008297:Male; D018482:Muscle, Skeletal / Q000737:chemistry / Q000276:immunology / Q000293:injuries* / Q000378:metabolism*; D016877:Oxidants / Q000378:metabolism*; D009195:Peroxidase / Q000378:metabolism; D011506:Proteins / Q000032:analysis; D011817:Rabbits; D013314:Stress, Mechanical; D013482:Superoxide Dismutase / Q000378:metabolism; D013746:Tetany / Q000378:metabolism; D013997:Time Factors; D019415:Torque; D014969:Xanthine Oxidase / Q000378:metabolism
chemical_list: D000975:Antioxidants; D016877:Oxidants; D011506:Proteins; D009195:Peroxidase; D013482:Superoxide Dismutase; D014969:Xanthine Oxidase