Oxidative Medicine and Cellular Longevity / 2018 / Article / Fig 4

Research Article

Parathyroid Hormone Causes Endothelial Dysfunction by Inducing Mitochondrial ROS and Specific Oxidative Signal Transduction Modifications

Figure 4

MitoTEMPO but not calcipotriol limits PTH-dependent ROS surge (a–d). The antioxidant properties of either calcipotriol or MitoTEMPO were tested on mitochondrial and total ROS productions in response to PTH (0.1 nM). BAECs were pretreated with calcipotriol (100 nM), stimulated with PTH at the same time, and as described above, mROS (a) and tROS (b) were determined. The data of fluorescence intensity were expressed as % increment vs. control and reported as mean ± SD. In another set of experiments, BAECs were pretreated with MitoTEMPO (5 μM), stimulated 30 min later with PTH, and as described above, mROS (c) and tROS (d) were determined. The data of fluorescence intensity were expressed as fold change vs. control whose mean value was set as 1 ( vs. CTRL). All images are the mean of three independent experiments.
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