Endotoxin, Epinephrine, and Ellagic Acid Effects on the Radiation-Sensitized Walker 256 Rat Carcinosarcoma

A radiation exposure of 1500 R to the Walker 256 rat tumor was found to sensitize this tumor to the effect of a sublethal dose of endotoxin (Sarratia marcescens lipopolysaccharide) given 2 days later so that complete or almost complete destruction of the tumor resulted. Histological study showed rap...

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Bibliographic Details
Published in:Radiation research 1968-10, Vol.36 (1), p.166-179
Main Authors: Ma. De Los Angeles Contreras, Bale, William F.
Format: Article
Language:English
Subjects:
Animals
Antibodies
Antineoplastics
Blood
Cancer
Carcinoma - drug therapy
Carcinoma - pathology
Carcinoma - radiotherapy
Combined Modality Therapy
Dosage
Dose-Response Relationship, Drug
Ellagic Acid - administration & dosage
Endotoxins
Endotoxins - administration & dosage
Epinephrine - administration & dosage
Female
Histology
Necrosis
Radiation Tolerance - drug effects
Rats
Rats, Sprague-Dawley
Space life sciences
Treatment Outcome
Tumors
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Summary:A radiation exposure of 1500 R to the Walker 256 rat tumor was found to sensitize this tumor to the effect of a sublethal dose of endotoxin (Sarratia marcescens lipopolysaccharide) given 2 days later so that complete or almost complete destruction of the tumor resulted. Histological study showed rapidly developing massive necrosis of tumor tissue. Tracer experiments with 131 I-labeled antibody to rat fibrin indicated an absence of blood circulation in the treated tumor. These results suggest that the lesion may be secondary to blood coagulation occurring in the vascular bed of the tumor. Apparently identical lesions were also produced by epinephrine and ellagic acid, alone or in combination. It is known that even untreated tumors are often the site of fibrin deposition. Presumably radiation, by injury to tumor cells, enhances the release of coagulation-producing substances into the vascular bed. It is postulated that the effect of subsequent treatment with the drugs listed above is produced by circulatory stasis induced in the tumor. This may be associated with Hageman factor activation or release of platelet factor 3.
ISSN:0033-7587
1938-5404
DOI:10.2307/3572548