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. 2013 May 24;1(1):292–296. doi: 10.1016/j.redox.2013.04.003

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Fig. 3 — Gene transfer of SOD3 protects aorta against XO-mediated vasomotor dysfunction. Following gene transfer of SOD3, (A) dose-dependent relaxation to ACh in the absence or presence of XO was determined. Gene transfer of β-galactosidase serves as negative control and exogenously applied bovine SOD (500 U/ml) serves as positive control. (n=6–10) ^⁎p<0.05 vs Adβgal without XO. (B) Maximal relaxation to ACh based on non-linear curve fit of data in (A). ^⁎p<0.05 vs Adβgal without XO; +p<0.05 Adβgal with XO. (C) EC50 relaxation to ACh based on non-linear curve fit of data in (A). (D) Lucigenin-enhanced chemiluminescence of xanthine/XO in the presence or absence of bovine SOD (n=3); p<0.05.