Figure 3.
Figure 3. Induction of ROS generation in Raji cells and the respiration-deficient subclones RajiC2, RajiC6, and RajiC8. Cells in exponential growing phase were incubated with Hu1D10 (5 μg/mL) without the cross-linking antibody for the indicated time. Cellular superoxide radical content was determined by flow cytometry analysis using dihydroethidium dye. The results show that Hu1D10 was able to cause a significant increase of ROS in both the wild-type (wt) and respiration-deficient cells (C2, C6, and C8), suggesting that the drug-induced ROS generation was not from within the mitochondrial respiratory chain.

Induction of ROS generation in Raji cells and the respiration-deficient subclones RajiC2, RajiC6, and RajiC8. Cells in exponential growing phase were incubated with Hu1D10 (5 μg/mL) without the cross-linking antibody for the indicated time. Cellular superoxide radical content was determined by flow cytometry analysis using dihydroethidium dye. The results show that Hu1D10 was able to cause a significant increase of ROS in both the wild-type (wt) and respiration-deficient cells (C2, C6, and C8), suggesting that the drug-induced ROS generation was not from within the mitochondrial respiratory chain.

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