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. Author manuscript; available in PMC: 2011 Feb 1.
Published in final edited form as: Biochim Biophys Acta. 2009 Nov 24;1797(2):285–295. doi: 10.1016/j.bbabio.2009.11.005

Fig. 4. Glutathione depletion does not affect mitochondrial function but potentiates diamide-induced cell death.

Fig. 4

(A) Cells were treated with buthionine sulfoximine (BSO; 0 – 1 mM) for 24 h and free glutathioine was measured by glutathione recycling assay. N ≥ 3 per group, *p < 0.05 vs. cells not treated with BSO. (B) Mitochondrial function in glutathione-depleted cells: Cells were treated with 0 (closed squares), 0.05 (open squares; dashed line), or 0.5 (open squares; dotted line) mM BSO for 24 h followed by mitochondrial function assay. After three baseline measurements of oxygen consumption rate (OCR), oligomyin (O; 1 µg/ml), FCCP (F; 1 µM), and antimycin A (A; 10 µM) were injected sequentially, and rates of oxygen consumption were recorded after each injection. (C) Glycolytic flux in glutathione-depleted cells: After 24 h of 0 (closed squares), 0.05 (open squares; dashed line), or 0.5 (open squares; dotted line) mM BSO treatment, baseline and oligomycin-stimulated extracellular acidification rates (ECAR) were measured. Inset: At the point shown by the arrow, the rate of extracellular was plotted for cells treated with 0–1 mM BSO. (D) Viability of normal (closed circles) and glutathione-depleted (open circles) cells treated with 0–0.25 mM diamide. N ≥ 3, and *p < 0.05 vs. diamide-treated cells not treated with BSO.