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. Author manuscript; available in PMC: 2024 Jan 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2022 Nov 3;43(1):79–91. doi: 10.1161/ATVBAHA.121.317735

Figure 1. Platelet SOD2 deficiency increases mitochondrial oxidants as well as total cellular ROS within platelets in aged mice.

Figure 1.

Washed platelets were prepared from young or aged mice deficient in platelet SOD2 (pSOD2-KO) or littermate controls. A. Mitochondrial pro-oxidant was detected by incubating platelets with 10 μM of MitoSox either at resting condition (RP) or in the presence of thrombin (Thr) and convulxin (Con). B. Levels of intracellular prooxidant detected by oxidation of dihydroethidium (DHE Fluorescence) measured in platelets at resting state (RP) or upon stimulation with thrombin and convulxin. C-E. Levels of intracellular ROS detected by oxidation of CM-H2DCF (DCF Fluorescence) was measured in platelets at resting state (RP) or upon stimulation with thrombin or convulxin or both. All the samples were analyzed by flow cytometry. Data for A and B are presented as median with 95% CI and analyzed by Kruskal-Wallis test with Dunn’s post hoc test for multiple group comparisons within each treatment group. Data for C-E are presented as mean ± SE and analyzed using two-way ANOVA with Tukey’s analysis for multiple group comparisons within each treatment. All the comparisons shown are for equivalent doses of agonists. N = 4–10 per group.