Oxidative Medicine and Cellular Longevity / 2018 / Article / Fig 3

Research Article

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

Figure 3

Evaluation of ROS production in response to PTH (a–f). BAECs were treated for 1 or 3 h with PTH (0.1 nM), and the total amount of ROS was determined incubating the cells with the fluorescent probe H2DCFDA. The fluorescence intensity was determined by citofluorimetry. The fluorescence relative to ROS levels was expressed as fold change vs. controls, whose mean value was set as 1 ( vs. CTRL). The image is the mean of three independent experiments (a). Representative images of flow cytometry of three independent experiments, evaluating tROS at 1 h (b) and 3 h (c) post-PTH treatment. The levels of mROS were determined in the same experimental condition, using Mitosox as specific fluorescent probe. The fluorescence relative to mROS levels was expressed as fold change vs. controls whose mean value was set as 1 ( vs. CTRL). The image is the mean of three independent experiments (d). Representative images of flow cytometry of three independent experiments, evaluating mitochondrial levels of ROS at 1 h (e) and 3 h (f) post-PTH treatment.
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