title: The influence of low-level laser therapy on parameters of oxidative stress and DNA damage on muscle and plasma in rats with heart failure.
abstract: In heart failure (HF), there is an imbalance between the production of reactive oxygen species and the synthesis of antioxidant enzymes, causing damage to the cardiovascular function and increased susceptibility to DNA damage. The aim of this study was to evaluate the influence of low-level laser therapy (LLLT) on parameters of oxidative stress and DNA damage in skeletal muscle and plasma of rats with HF. Wistar rats were allocated into six groups: "placebo" HF rats (P-HF, n = 9), "placebo" Sham rats (P-sham, n = 8), HF rats at a dose 3 J/cm(2) of LLLT (3 J/cm(2)-HF, n = 8), sham rats at a dose 3 J/cm(2) of LLLT (3 J/cm(2)-sham, n = 8), HF rats at a dose 21 J/cm(2) of LLLT (21 J/cm(2)-HF, n = 8) and sham rats at a dose 21 J/cm(2) of LLLT (21 J/cm(2)-sham, n = 8). Animals were submitted to a LLLT protocol for 10 days at the right gastrocnemius muscle. Comparison between groups showed a significant reduction in superoxide dismutase (SOD) activity in the 3 J/cm(2)-HF group (p = 0.03) and the 21 J/cm(2)-HF group (p = 0.01) compared to the P-HF group. 2',7'-Dihydrodichlorofluorescein (DCFH) oxidation levels showed a decrease when comparing 3 J/cm(2)-sham to P-sham (p = 0.02). The DNA damage index had a significant increase either in 21 J/cm(2)-HF or 21 J/cm(2)-sham in comparison to P-HF (p = 0.004) and P-sham (p = 0.001) and to 3 J/cm(2)-HF (p = 0.007) and 3 J/cm(2)-sham (p = 0.037), respectively. Based on this, laser therapy appears to reduce SOD activity and DCFH oxidation levels, changing the oxidative balance in the skeletal muscle of HF rats. Otherwise, high doses of LLLT seem to increase DNA damage.
authors.affiliation: Laboratory of Experimental Physiology, Universidade Federal de Ciências da Saúde de Porto Alegre, Porto Alegre, RS, Brazil.
authors.forename: Micheli
authors.initials: M
authors.lastname: Biasibetti
authors.forename: Denise B
authors.initials: DB
authors.lastname: Rojas
authors.forename: Vítor S
authors.initials: VS
authors.lastname: Hentschke
authors.forename: Dinara Jaqueline
authors.initials: DJ
authors.lastname: Moura
authors.forename: Marlus
authors.initials: M
authors.lastname: Karsten
authors.forename: Clóvis M D
authors.initials: CM
authors.lastname: Wannmacher
authors.forename: Jenifer
authors.initials: J
authors.lastname: Saffi
authors.forename: Pedro
authors.initials: P
authors.lastname: Dal Lago
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D004249:DNA Damage; D005452:Fluoresceins / Q000737:chemistry; D005979:Glutathione Peroxidase / Q000378:metabolism; D006333:Heart Failure / Q000532:radiotherapy*; D006439:Hemodynamics; D007249:Inflammation / Q000378:metabolism; D007834:Lasers; D028022:Low-Level Light Therapy / Q000379:methods*; D008297:Male; D018482:Muscle, Skeletal / Q000528:radiation effects*; D018384:Oxidative Stress; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: C109098:2,7-dihydrodichlorofluorescein diacetate; D000975:Antioxidants; D005452:Fluoresceins; D017382:Reactive Oxygen Species; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase