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. Author manuscript; available in PMC: 2007 Aug 14.
Published in final edited form as: J Biol Chem. 2002 Sep 5;277(45):43377–43388. doi: 10.1074/jbc.M206373200

Fig. 2. The effect of cisplatin on F0F1-ATPase activity (A) and intracellular ATP content (B).

Fig. 2

A, RPTC were treated with 50 μm cisplatin and mitochondria were isolated at 1, 2, 4, 8, 12, 18, and 24 h of cisplatin exposure. The F0F1-ATPase activity assay was performed at 31 °C in 10 mm Tris-HCl, pH 8.2, containing 200 mm KCl, 3 mm MgCl2, and RPTC mitochondria. The reaction was initiated by the addition of ATP (5 mm) and terminated after 5 min by adding 3 m trichloroacetic acid to precipitate protein. The inorganic phosphate concentration in the supernatant was determined using Sumner reagent. Each mitochondrial sample was run in the absence and presence of oligomycin (10 μg/ml), and the F0F1-ATPase activity was expressed as the oligomycin-sensitive phosphate production. Results are the average ± S.E. of three experiments (RPTC isolations). B, RPTC were treated with 50 μm cisplatin and samples were taken at 1, 2, 4, 8, 18, and 24 h of cisplatin exposure for measurements of intracellular ATP content. Results are the average ± S.E. of five experiments (RPTC isolations).