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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) <t>EC50</t> 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.
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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) <t>EC50</t> 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.
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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) <t>EC50</t> 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.
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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) <t>EC50</t> 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.
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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) <t>EC50</t> 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.
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Image Search Results


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.

Journal: Redox Biology

Article Title: Extracellular but not cytosolic superoxide dismutase protects against oxidant-mediated endothelial dysfunction

doi: 10.1016/j.redox.2013.04.003

Figure Lengend Snippet: 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.

Article Snippet: A non-linear curve fit (3 parameter with a Hill slope of 1.0) was used to determine the maximal and EC50 relaxation (GraphPad Prism for Windows).

Techniques: Negative Control, Positive Control

Gene transfer of SOD1 does not protect against XO-mediated vasomotor dysfunction. Following gene transfer of SOD1, (A) dose-dependent relaxation to ACh in the absence or presence of XO was determined as described for . ⁎ p <0.05 vs Adβgal without XO. (B) Maximal relaxation and (C) EC50 to ACh based on non-linear curve fit of data in (A). ⁎ p <0.05 vs Adβgal without XO;+ p <0.05 Adβgal+SOD+XO.

Journal: Redox Biology

Article Title: Extracellular but not cytosolic superoxide dismutase protects against oxidant-mediated endothelial dysfunction

doi: 10.1016/j.redox.2013.04.003

Figure Lengend Snippet: Gene transfer of SOD1 does not protect against XO-mediated vasomotor dysfunction. Following gene transfer of SOD1, (A) dose-dependent relaxation to ACh in the absence or presence of XO was determined as described for . ⁎ p <0.05 vs Adβgal without XO. (B) Maximal relaxation and (C) EC50 to ACh based on non-linear curve fit of data in (A). ⁎ p <0.05 vs Adβgal without XO;+ p <0.05 Adβgal+SOD+XO.

Article Snippet: A non-linear curve fit (3 parameter with a Hill slope of 1.0) was used to determine the maximal and EC50 relaxation (GraphPad Prism for Windows).

Techniques: