The effect of 2, 4-dinitrophenol and of fluoride on oxidations in normal and tumor tissues.

Summary The capacity and the lability of the coupled oxidative phosphorylation systems of liver, kidney, and of seven different tumors have been investigated with the aid of DNP and of fluoride, which act to stimulate and to inhibit, respectively, the net breakdown of high-energy phosphate. No over-all oxidative pattern common to tumor homogenates has been observed. The great difference in oxidative response among various tumors has been emphasized, and the results have been considered to represent the contribution of the tissue of origin to the enzyme pattern of the tumor tissues, and to reflect the multiplicity of enzyme patterns seen in normal growing and nongrowing tissues. The significance of the findings was discussed in relation to the problem of finding the balance between anabolic and catabolic pathways that involve the same substrates.

[1]  P. Siekevitz,et al.  Intramitochondrial regulation of oxidative rate. , 1953, The Journal of biological chemistry.

[2]  V. Potter,et al.  Studies on tissue metabolism by means of in vivo metabolic blocking technics. II. Metabolism of acetate-1-C14 in malonate-treated rats. , 1953, Cancer research.

[3]  P. Siekevitz,et al.  The adenylate kinase of rat liver mitochondria. , 1953, The Journal of biological chemistry.

[4]  S. Weinhouse,et al.  Metabolism of neoplastic tissue. III. Diphosphopyridine nucleotide requirements for oxidations by mitochondria of neoplastic and non-neoplastic tissues. , 1953, Cancer research.

[5]  H. Lardy,et al.  Influence of potassium and other alkali cations on respiration of mitochondria. , 1952, The Journal of biological chemistry.

[6]  M. P. Lenta,et al.  The coenzyme I oxidase system in normal and tumor tissues. , 1952 .

[7]  E. P. Kennedy,et al.  Oxidative phosphorylation catalyzed by cytoplasmic particles isolated from malignant tissues. , 1952, Cancer research.

[8]  R. K. Kielley.  Oxidative phosphorylation by mitochondria of transplantable mouse hepatoma and mouse liver. , 1952, Cancer research.

[9]  S. Weinhouse,et al.  Metabolism of neoplastic tissue. II. A survey of enzymes of the citric acid cycle in transplanted tumors. , 1952, Cancer research.

[10]  S. Weinhouse.  Studies on the fate of isotopically labeled metabolites in the oxidative metabolism of tumors. , 1951, Cancer research.

[11]  V. Potter.  Studies on the reactions of the Krebs citric acid cycle in tumor, with homogenates, slices, and in vivo technics. , 1951, Cancer research.

[12]  W. C. Schneider,et al.  Oxidative phosphorylation in whole homogenates and in cell particles. , 1951, The Journal of biological chemistry.

[13]  V. Potter,et al.  Oxidative phosphorylation in homogenates of normal and tumor tissues. , 1951, Cancer research.

[14]  V. Potter,et al.  Citric acid content of normal and tumor tissues in vivo following injection of fluoroacetate. , 1950, Cancer research.

[15]  G. Lepage.  A comparison of tumor and normal tissues with respect to factors affecting the rate of anaerobic glycolysis. , 1950, Cancer research.

[16]  S. Weinhouse,et al.  OCCURRENCE OF THE CITRIC ACID CYCLE IN TUMORS , 1950 .

[17]  A. Pardee,et al.  Factors affecting the maintenance of oxidative phosphorylation in a kidney homogenate system. , 1949, The Journal of biological chemistry.

[18]  O. H. Lowry,et al.  The determination of inorganic phosphate in the presence of labile phosphate esters. , 1946, The Journal of biological chemistry.

[19]  G. Youngburg.  Phosphorus Metabolism , 1932 .