UV microspectrophotometry of mitochondrial responses to extracellular glucose in cultured ascites tumor cells.

  title={UV microspectrophotometry of mitochondrial responses to extracellular glucose in cultured ascites tumor cells.},
  author={C. Ritter and B. Thorell},
  journal={Experimental cell research},
  volume={65 1},
Summary Extracellular glucose addition to cultured ascites cells is followed by a decrease in UV absorption of intracellular mitochondria. Dicumarol also produces a decrease in such UV absorption and, following a maximum effect, addition of glucose is ineffective. Deoxyglucose reversibly inhibits the effect of glucose. It is proposed that the mitochondrial UV absorbing material, which is lost following extracellular glucose addition, is adenine nucleotide and that the adenine nucleotide loss is… 
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Calcium transport in intact Ehrlich ascites tumor cells.
Ca 2+ transport by both intact ascites tumor cells and ascites cell mitochondria was studied spectrophotometrically using murexide, a metallochronic indicator of Ca 2+ concentrations to indicate that ascite tumor cells possess a plasma membrane permeable to Ca 2+, and that the Ca 1+ uptake by mitochondria inside the cell accounts for the entire cellular Ca 2- accumulation.
A two-channel microfluorometric method for the analysis of metabolic interactions and transport phenomena in the intact cell
Two-channel microfluorometry opens the way to a detailed exploration of unknown or unsuspected patterns of metabolic interactions and intracellular regulation.
Microspectroscopy and Flow Cytometry
Publisher Summary This chapter discusses the involvement of Bo Thorell in the development of microspectroscopy. Thorell's had a deep curiosity in the dynamics of cell function. Thorell developed the


  • C. Ritter, B. Thorell
  • Chemistry, Medicine
    The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
  • 1970
It is proposed that the main factor responsible for the large decrease in 265 mµ absorption is adenine nucleotide loss, which is more than would be expected based on the increase in absorption seen at 330-340mµ.
Theoretical phosphorylation rates after addition of a small amount of glucose to intact ascites tumor cells.
The low rate of change in the ATP content of the cells indicated that most of the change in phosphorylation rate represented changes in both ATP synthesis and ATP utilization, and it is hypothesized that ATP synthesized by glycolysis is more readily available to the ATP-utilizing systems.
Microspectrography of respiratory enzymes within the single, mammalian cell under different metabolic conditions.
Microspectrographic techniques have been developed which permit measurements of specific absorptions of about a per cent in the long-wave ultraviolet and visible wavelength region from intact, living-cell areas of 1.5 μ in diameter, and showed that the metabolic state of the respiratory system of small parts in the single, intact mammalian cell could be analyzed.
Kinetic evidence for multiple binding sites on phosphofructokinase.
Abstract For brain phosphofructokinase at pH 8, with noninhibitory levels of adenosine triphosphate, the Michaelis constants for ATP (0.1 mm) and fructose-6-P (0.04 mm) are each independent of the
Studies on heart phosphofructokinase. Binding properties of native enzyme and of enzyme desensitized to allosteric control.
The binding properties of purified sheep heart phosphofructokinase were studied with a gel filtration technique and were compared with those of enzyme desensitized to allosteric control by photooxidation to show the effect of different enzyme effectors on the binding of the above mentioned substrates.
Cross-reactions of adenosine 3',5'-monophosphate-dependent protein kinase systems from rat liver and rabbit skeletal muscle.
Protein kinases and regulatory proteins (R-proteins) which are capable of binding adenosine 3',5'-monophosphate (cyclic AMP) are partially purified from rat liver and rabbit skeletal muscle soluble
Low-temperature spectroscopy of ascites cells and mitochondria.
Metabolic control mechanisms. I. Electron transfer in the mammalian cell.