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Effect of Various Drugs on the Tumor-necrotizing Activity of Several Chemical Agents in Mice^*

Sachindra N. Pradhan, Betty Achinstein and Murray J. Shear

( National Cancer Institute, Bethesda, Md.)

The inhibitory effect of a number of drugs on the hemorrhagic necrosis induced in tumors with several agents was examined in CAF₁ mice bearing Sarcoma 37, with the following findings:

1. S. marcescens polysaccharide.—The tumornecrotizing potency of the bacterial polysaccharide from S. marcescens was reduced by dibenamine, dibenzyline, priscoline, cortisone, and urethan; surgery under urethan anesthesia inhibited tumor damage more than did urethan alone; regitine, dihydroergotamine, pentobarbital sodium, and phenobarbital sodium did not show any inhibitory effect.

2. Pitressin.—Atropine, dibenamine, dibenzyline and phenobarbital sodium inhibited, in varying degree, pitressin-induced tumor damage; cortisone and pentobarbital sodium had no effect.

3. Serotonin.—Dibenzyline, dibenamine, and priscoline inhibited to some extent the tumor damage induced by serotonin; the other supplementary drugs did not.

4. Amphetamine.—Dibenzyline and urethan inhibited the tumor-necrotizing effect of amphetamine; its lethal toxicity was increased by atropine.

5. Histamine.—Tumor-necrosis induced by histamine was inhibited by atropine, dibenamine, dibenzyline, and, to some extent, by pentobarbital sodium; cortisone and phenobarbital sodium had no effect.

6. Acetylpodophyllotoxin--pyridinium chloride.—The tumor-necrotizing effect of acetylpodophyllotoxin--pyridinium chloride was not affected by any of the drugs used.

^* A preliminary report was published in J. Pharmacol. & Exper. Therap., 116:47, 1956, in the Proceedings of the 1955 Fall meeting at Iowa of the American Society for Pharmacology and Experimental Therapeutics.

Present address: Department of Pharmacology, Howard University School of Medicine, Washington, D.C.

Received 7/26/56.