Figure 2.

Mitochondria are a potential source of increased ROS in PVAT from obese mice, and mitochondria‐derived ROS alter the expression of antioxidant enzymes in PVAT. Concentration–effect curves to PE were performed in endothelium‐denuded aortic rings from control [(A and C) n = 8 for each experimental group] and obese [(B and D) n = 8 for each experimental group] mice. The role of mROS on PVAT modulation of aortic smooth muscle contraction was investigated using MnTMPyP (3 × 10⁻⁵ M), a mitochondria‐targeted superoxide scavenger and PEG‐catalase (Peg‐cat; 200 U·mL⁻¹), which dismutates mitochondria‐derived H₂O₂. Protein expression and activity of the antioxidant enzymes SOD‐Mn [(E and G) n = 5 in both groups] and catalase [(F and H) n = 5 in both groups] were determined by Western blot and SOD‐Mn and catalase activity assay kits, respectively, in PVAT from control and obese mice. Representative Western blots are shown in the upper panels, with quantitative analysis in the lower panels. Results were normalized to β‐actin expression and are expressed as relative units. Results represent the mean ± SEM. ^* P < 0.05 versus Control PVAT (+); ^# P < 0.05 versus Obese PVAT (+); ^& P < 0.05 versus Obese PVAT (−); ^π P < 0.05 versus Control.