Oxidative phosphorylation and ATPase activities of human tumor mitochondria.
Studies were carried out with intact mitochondria isolated from human astrocytoma, oat cell carcinoma and melanoma which were propagated in athymic mice. These human tumor mitochondria were capable of coupled oxidative phosphorylation. They also showed significant uncoupler-stimulated ATPase if defatted bovine serum albumin was included in the assay media. However, the uncoupler response curves were different and the magnitude of the ATPase activity was lower than could be obtained with mitochondria of a normal tissue, such as liver. Some of these characteristics were also exhibited by mitochondria from several animal hepatomas and Ehrlich ascites tumor. In the three tumors studied, mitochondria from oat cell carcinoma were more labile, whereas higher respiratory control ratios and greater stimulation of ATPase by uncouplers were obtained with melanoma mitochondria. The mitochondrial ATPase was not the major cellular ATPase in any of the three tumors. This was indicated by a low inhibition of the ATPase activity of tumor cell homogenates by oligomycin. A very large fraction of the cellular ATPase activities was recovered in the microsomal fractions.
D000251:Adenosine Triphosphatases / Q000378:metabolism*; D000818:Animals; D001254:Astrocytoma / Q000378:metabolism*; D002258:Carbonyl Cyanide m-Chlorophenyl Hydrazone / Q000494:pharmacology; D018288:Carcinoma, Small Cell / Q000378:metabolism*; D004140:Dinitrophenols / Q000494:pharmacology; D006801:Humans; D007700:Kinetics; D008545:Melanoma / Q000378:metabolism*; D051379:Mice; D008819:Mice, Nude; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism*; D009368:Neoplasm Transplantation; D010085:Oxidative Phosphorylation / Q000187:drug effects; D014183:Transplantation, Heterologous
D004140:Dinitrophenols; D002258:Carbonyl Cyanide m-Chlorophenyl Hydrazone; D000251:Adenosine Triphosphatases