Hydrogen peroxide (H2O2) is not increased in angiotensin II (AngII)stimulated neurons overexpressing superoxide dismutase (SOD) Academic Article uri icon


  • Previous studies have shown that SOD overexpression in neurons inhibits AngII intraneuronal signaling; thus, suggesting that superoxide radicals (O2) are key signaling intermediates driving AngIIinduced neuronal activation. However, considering H2O2 is a direct product of O2 dismutation by SOD, an alternative interpretation is that increased H2O2 mediates the inhibition of AngII signaling in SOD overexpressing neurons. We aimed to determine if H2O2 levels are indeed increased in SOD overexpressing neurons stimulated with AngII. To query this, we used a neuronal cell culture model expressing HyPer, a H2O2sensitive fluorescent protein. To determine the sensitivity of HyPer to H2O2, neurons were stimulated with increasing concentrations of H2O2 (1100 M) and changes in HyPer fluorescence were observed by realtime confocal imaging. Robust increases in HyPer fluorescence were detected after treatment of 5 M, but not after 1 M H2O2. In contrast, no changes in HyPer fluorescence were observed after AngII (100 nM) stimulation in control or SOD overexpressing neurons. These data suggest that AngII does not increase H2O2 levels in SOD overexpressing neurons, or does so at concentrations below the level of HyPer detection. These data further support the hypothesis that SOD overexpression inhibits AngII intraneuronal signaling by decreasing O2 levels, but not by increasing H2O2 levels. AHA 0930204N.

published proceedings

  • The FASEB Journal

author list (cited authors)

  • Case, A. J., Cruz, R. F., & Zimmerman, M. C.

citation count

  • 0

complete list of authors

  • Case, Adam J||Cruz, Rodrigo Franco||Zimmerman, Matthew C

publication date

  • April 2013