The three colors were merged together. Original magnification, ×400. (B) Intracellular cadmium mass in cells after exposure to QDs with different surface modifications
for 24 h was analyzed by ICP-MS (n = 3). It was reported that GO exposure led to PLX-4720 ic50 cytotoxicity to macrophages . It was also documented that GO GDC-0973 ic50 could cause hemolysis in vitro. Thus far, the biological performance of GO on erythroid progenitor cells has not been investigated. We here assessed the impact of GO exposure on primary E14.5 fetal liver cells, which are predominantly erythroid progenitor cells with a small portion of other types of cells, such as macrophages [19, 27, 28]. GO provoked the substantial cell death of E14.5 fetal liver cells via apoptosis, as shown in Figure 5A,
the percentages of Q4 (early apoptosis) plus Q2 (late apoptosis) were significantly increased in GO-treated cells (at 20 μg/ml, P < 0.05) compared to the control cells. Overall, the apoptotic cells (Annexin V+) increased considerably upon exposure to GO in comparison to the this website control cells (29.9% vs. 49.2%, Figure 5A, P < 0.05). It should be noted that in spite of only a small proportion of macrophages in fetal liver, they are indispensable for fetal erythropoiesis involving the establishment of erythroblastic islands . We also observed a slight increase of necrosis in fetal liver cells treated with GO (Figure 5A), which was presumably due to the difference of fetal liver macrophages from erythroid
cells Clostridium perfringens alpha toxin in terms of their process of death (i.e., necrosis for macrophages upon GO treatment). Figure 5 GO-triggered cell death of erythroid cells through apoptosis. (A) Representative FACS images describing fetal liver cell death upon GO treatment at 20 μg/ml for 24 h using Annexin V and PI staining. (B) FACS analysis of relative fluorescent intensity reflecting ROS content after GO exposure at various concentrations at different time points in fetal liver cells. ANOVA was used to determine the mean difference in cells treated with GO at different concentrations and along time course compared to control. Our recent study suggested that sodium arsenite induced substantial oxidative stress (ROS synthesis), resulting in apoptosis on erythroid cells . We therefore assessed the intracellular ROS level in fetal liver cells after GO treatment. As shown in Figure 5B, the DCF fluorescent intensity was greatly enhanced in fetal liver cells treated with GO at various concentrations for only 15 min (Figure 5B, P < 0.001). The clear shift of DCF fluorescent peak continued at 0.5, 1, and 6 h (Figure 5B, P < 0.001). These results together suggested that GO-induced apoptosis in erythroid cells was likely dependent on ROS-mediated oxidative stress, similar to the mechanism responsible for arsenic-stimulated apoptosis in erythroid cells .