Fig. 5: CKMT1 deficiency increased mitochondrial ROS via RET. | Cell Death & Disease

Fig. 5: CKMT1 deficiency increased mitochondrial ROS via RET.

From: CKMT1 deficiency contributes to mitochondrial dysfunction and promotes intestinal epithelial cell apoptosis via reverse electron transfer-derived ROS in colitis

Fig. 5

After treated with TNF-α for 24 h (50 ng/ml), DCFH-DA staining showing cellular ROS levels in (A) Lovo cell, or (B) NCM460 cells, via flow cytometry. After treated with TNF-α for 24 h, MitoSOX staining of mitochondrial ROS (mtROS) was assessed via C flow cytometry in Lovo cells, or D via fluorescence microscopy in NCM460 cells. E The effects of FCCP (100 nM) or diazoxide (200 nM) pretreatment on TNF-α-induced mtROS in siCK Lovo cells were assessed via flow cytometry. F The mtROS levels were measured by flow cytometry in Lovo cells pretreated with rotenone (10 nM). G Illustration of electron transport chain-derived ROS production at complex I via RET. H AOX expression markedly reduced the TNF-α-induced mtROS levels in siCK cell. I NADH/NAD+ ratio was measured in cell lysis via microplate reader (n = 3 or 4), and J MMP (stained with TMRE) was measured via flow cytometry. All flow cytometry experiments were repeated three times. *P < 0.05; **P < 0.01; ***P < 0.001.

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