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Effect of Endotoxin on Liver Carbohydrate of Mice Bearing Transplantable Tumors Sarcoma 37 and Krebs-2 Carcinoma^*

H. Francis Havas, L. Joe Berry and Dorothy S. Smythe

( Department of Microbiology, Temple University School of Medicine, and the Institute for Cancer Research, Philadelphia, Pennsylvania, and the Department of Biology, Bryn Mawr College, Bryn Mawr, Pennsylvania)

A comparison is made between the stability of carbohydrate in the liver of normal mice and of mice bearing the transplantable tumors, Sarcoma 37 or Krebs-2 carcinoma. Although the presence of the tumor does not alter the level of liver carbohydrate it sensitizes the animal to endotoxin. Thus, liver carbohydrate is depleted in tumor-bearers by one-tenth as much endotoxin as is required for a similar change in normal animals.

Surgical removal of Sarcoma 37 restores normal stability in liver carbohydrate within a period of 48 hours.

Cortisone "protects" the carbohydrate in animals of each type (tumor-bearers and controls) from depletion by endotoxin, whereas Proferrin (colloidal saccharated iron oxide) greatly sensitizes the tumor-bearing mice to this effect of endotoxin.

Assays for liver tryptophan pyrrolase showed higher activities in tumor-bearing mice than in controls. A small dose of endotoxin raised the enzyme level in control mice but depressed it in tumor-bearing animals. Ten times as much endotoxin was required to produce a comparable depression of the enzyme in control mice.

The LD₅₀ of endotoxin was less in tumor-bearing mice than in controls, but it was elevated in both groups by cortisone, nicotinamide, and diphosphopyridine nucleotide and lowered by Proferrin.

The biochemical effects of tumors on host tissues and their relationship to other conditions of stress are discussed.

^* This work was supported at The Institute for Cancer Research, in part by Grant CY-2976-CY from the National Cancer Institute, National Institutes of Health, Public Health Service, in part by a grant from the New York Cancer Research Institute, Inc., and in part by an Institutional Grant from the Institute for Cancer Research; and at Bryn Mawr College by a National Science Foundation Grant (NSF-GB 774) and by Contract AF 41 (609)-1764 between Bryn Mawr College and the Arctic Aeromedical Laboratory, United States Air Force.

Present address: Department of Microbiology, Temple University School of Medicine, Philadelphia, Pa.

Received 6/ 9/64.