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. Author manuscript; available in PMC: 2011 Jan 11.
Published in final edited form as: J Cardiovasc Pharmacol. 2010 Apr;55(4):308–316. doi: 10.1097/fjc.0b013e3181d89670

Figure 3.

Figure 3

Tyrosine nitration and inactivation of MnSOD in diabetic apoliprotein E deficient mice is prevented by TP antagonist. Upper panels show examples of immunohistochemical staining of kidneys of atherosclerotic, hyperlipidemic apolipoprotein E deficient mice that were given type-1 diabetes by administration of streptozotocin. The red staining was achieved with a sequence-specific antibody that detects nitration of tyrosine-34 of MnSOD74. Treatment of the mice with the TP antagonist, S18886 restored staining to a level indistinguishable from that in non-diabetic control mice, whereas aspirin had no significant effect. The bar graph shows that the renal MnSOD enzymatic activity was significantly decreased from control in the diabetic mice, and that treatment with S18886, but not aspirin prevented the decrease. Data from reference 64.