POLYHYDRIC ALCOHOL PRODUCTION BY OSMOPHILIC YEASTS: STUDIES WITH C14-LABELED GLUCOSE

1956 ◽  
Vol 34 (3) ◽  
pp. 495-501 ◽  
Author(s):  
J. F. T. Spencer ◽  
A. C. Neish ◽  
A. C. Blackwood ◽  
H. R. Sallans

D-Glucose was dissimilated aerobically by a strain of osmophilic yeast producing glycerol, D-arabitol, ethanol, carbon dioxide, and a small amount of succinic acid. Glucose-1-C14 gave glycerol labeled in the terminal carbons, D-arabitol labeled in carbon-1 and carbon-5, methyl labeled ethanol, and succinic acid with 30% of the labeling in the carboxyl carbons and 70% in the methylene carbons. Glucose-2-C14 gave glycerol labeled in carbon-2, D-arabitol labeled in carbon-1, carbon-2, and carbon-4, carbinol labeled ethanol, and succinic acid having 70% of the labeling in the carboxyl carbons and 30% in the methylene carbons. Labeled carbon dioxide was produced from both carbon-1 and carbon-2 labeled glucose but the specific activity of carbon dioxide from glucose-1-C14 was higher than that from glucose-2-C14. The distribution of radioactive carbon in the products is explained by assuming that glucose is dissimilated via a combination of the Embden–Meyerhof and the phosphogluconate oxidation pathways, with transketolase-catalyzed reactions playing an important part in D-arabitol formation.

1956 ◽  
Vol 34 (1) ◽  
pp. 495-501 ◽  
Author(s):  
J. F. T. Spencer ◽  
A. C. Neish ◽  
A. C. Blackwood ◽  
H. R. Sallans

D-Glucose was dissimilated aerobically by a strain of osmophilic yeast producing glycerol, D-arabitol, ethanol, carbon dioxide, and a small amount of succinic acid. Glucose-1-C14 gave glycerol labeled in the terminal carbons, D-arabitol labeled in carbon-1 and carbon-5, methyl labeled ethanol, and succinic acid with 30% of the labeling in the carboxyl carbons and 70% in the methylene carbons. Glucose-2-C14 gave glycerol labeled in carbon-2, D-arabitol labeled in carbon-1, carbon-2, and carbon-4, carbinol labeled ethanol, and succinic acid having 70% of the labeling in the carboxyl carbons and 30% in the methylene carbons. Labeled carbon dioxide was produced from both carbon-1 and carbon-2 labeled glucose but the specific activity of carbon dioxide from glucose-1-C14 was higher than that from glucose-2-C14. The distribution of radioactive carbon in the products is explained by assuming that glucose is dissimilated via a combination of the Embden–Meyerhof and the phosphogluconate oxidation pathways, with transketolase-catalyzed reactions playing an important part in D-arabitol formation.


The breakdown of 14 C-labelled glucose, pyruvate and lactate to yield radioactive carbon dioxide has been studied in the blood of cats, rabbits and dogs incubated outside the body at 37°C. The process has been shown to be dependent upon access to oxygen and to be greatly depressed by cooling the incubation mixture to 0°C, or by previous beating of the blood to 100° C. The enzymic nature of the reactions involved is further indicated by the effects of a number of know n enzyme poisons. Fractionation of rabbit blood has demonstrated that the active elements in the production of radioactive carbon dioxide are the white cells, and it has been calculated that the rate of their oxidative metabolism can account for the complete breakdown of 0*3 mg glucose per 100 ml. of blood per hour. The finding that arsenite strongly inhibits the oxidation of pyruvate without greatly affecting that of glucose points to the operation of a direct oxidative pathway for glucose not involving the usual glycolytic series of intermediates, that is, the so-called ‘hexose-monophosphate shun t5. The idea that such a mechanism functions in the leucocytes is supported by the results of experiments with inhibitors other than arsenite, and by the observation that glucose labelled only in the 1-carbon atom is a richer source of radioactive carbon dioxide than uniformly labelled glucose of the same specific activity.


1941 ◽  
Vol 139 (1) ◽  
pp. 377-381 ◽  
Author(s):  
H.G. Wood ◽  
C.H. Werkman ◽  
Allan Hemingway ◽  
A.O. Nier

1961 ◽  
Vol 39 (11) ◽  
pp. 1717-1735 ◽  
Author(s):  
P. G. Scholefield

The cumulative entry of amino acids into Ehrlich ascites carcinoma cells is due to the presence of active transport systems, each with its own specific range of substrates. Several amino acids and amino acid analogues may have an affinity for the same transport system and thus may inhibit transport of other amino acids by acting as competitive inhibitors or competitive substrates. Loss of methionine from ascites cells takes place by a diffusion process which obeys Fick's law. Leucine accumulation by ascites cells is small and is increased on addition of certain other amino acids. The increase is not due to inhibition of leucine oxidation as increase in the rate of production of radioactive carbon dioxide from labeled leucine also occurs. Kinetic aspects of these results are discussed.


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