The inhibition of lactic acid formation in cancer and muscle / by Sylvia Thurlow Harrison and Edward Mellanby.

  • Harrison, Sylvia Thurlow.
Date:
[1930?]
Catalogue details

Licence: In copyright

Credit: The inhibition of lactic acid formation in cancer and muscle / by Sylvia Thurlow Harrison and Edward Mellanby. Source: Wellcome Collection.

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    acid formed, ranging from 20 to 100%. Warburg has shown that cancer tissue can use fructose also as a precursor of lactic acid. In the last two experiments in Table IV, 0-4 % fructose was used instead of glucose and it can be seen that pancreatic extract inhibits this glycolysis also. Barr, Ronzoni and Glaser [1928] quote a total of 21 manometric experi¬ ments on the glycolysis of cancer tissue in the presence of pancreatic extract, 8 cases of inhibition occurring, ranging from 6 to 37 %. They also give 6 chemical experiments in 2 of which inhibition occurred, to the extent of 5 and 29 % respectively. They conclude that pancreatic extract causes no appreciable inhibition in the glycolysis of cancer tissue. If all the experiments in the previous four tables are considered together (not counting the 3 in which the pancreatic extract had no amylase), there is a total of 63, with only 4 where no inhibition occurred. We feel justified, then, in stating that some factor, presumably amylase, common to pancreatic extract, malt diastase, takadiastase and dry salivary gland, does cause an inhibition in the glycolysis of the cancer tissue used in this laboratory. The question now arises as to the mechanism by which these various extracts bring about inhibition. McCullagh has shown that the substance which brings about the inhibition in muscle glycolysis when starch is used is amylase. After the publication of this work, tests for amylase were always made on the various extracts used in our work, and we found that extracts containing no amylase gave no inhibition in the glycolysis of cancer tissue. It is difficult to make any accurate comparison using cancer tissue between the degree of inhibition caused by various preparations and their amylase content, because the use of slices of tissue, rather than the homogeneous tissue extract which McCullagh used from muscle, involves an experimental error which invalidates any but fairly large differences. Barr, Ronzoni and Glaser made an extract of cancer tissue but found it to be glycolytically inactive. It is therefore, at the moment, impossible to work with a more homogeneous source of the glycolytic enzyme from cancer tissue than is provided by slices of tissue. We assume, then, for the time being, that the factor inhibiting glycolysis in cancer tissue is amylase. McCullagh claims that amylase inhibits the glycolysis of starch because it prevents the formation of hexosephosphate which is known to be an intermediate product in the breakdown by muscle of starch to lactic acid. Barr, Ronzoni and Glaser, who added phosphate to bicarbonate-Ringer, observed no increase in the lactic acid formation by cancer tissue, and hence they assumed that glucose, when acted upon by cancer tissue, did not go through a phos¬ phate stage. This assumption was supported by their inability to observe any changes in inorganic phosphorus during the course of glycolysis in cancer tissue. They therefore explain their observations that in the majority of cases pancreatic extract did not inhibit the glycolysis of cancer tissue, by agreeing with McCullagh as to the function of the inhibiting factor, namely that in muscle it prevents the formation of hexosephosphate. If, in cancer meta-