Impaired mitochondrial OXPHOS function in TSA-treated breast cancer cells.

<p>Exponentially growing MDA-MB-231 and MCF-7 cells were treated with DMSO (control) or 500 nmol/L of TSA. (<b>A</b>) Measurement of the mitochondrial complex I, II, III, IV and V activities exposure to TSA at 24 h (n = 3). Error bars indicated the SD; *P<0.05, **P<0.01 compared to DMSO treatment (control) using Student's t-test. (<b>B</b>) Expression of some subunits of mitochondrial complex I and complex III in response to TSA at 24 h. Representative of 3 experiments. (<b>C</b>) Oxygen consumption rate (OCR) in breast cancer cells treated with/without TSA for 24 h and sequentially exposed to (a) oligomycin, (b) FCCP, (c) rotenone and antimycin. Mean±SD, n = 5. (<b>D</b>) TMRE fluorescence as a measure of mitochondrial membrane potential (n = 3). Error bars indicated the SD; **P<0.01 compared to DMSO treatment in a Student's t-test. (<b>E</b>) Transmission electron microscopy showed differences in mitochondrial appearances. Δ indicated mitochondria. Scale bar = 500 nm. (<b>F</b>) ATP content (n = 6). Error bars indicated the SD; *P<0.05, **P<0.01 compared to DMSO treatment (control) using Student's t-test.