Ethanol increases tumor progression in rats: Possible involvement of natural killer cells

Raz Yirmiya*, Shamgar Ben-Eliyahu, Robert P. Gale, Yehuda Shavit, John C. Liebeskind, Anna N. Taylor

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

43 Scopus citations


The effects of acute and chronic ethanol administration on tumor progression and metastasis were studied in rat models of leukemia and breast cancer, respectively. Acute administration of 1.5-3.5 g of ethanol/kg body weight significantly reduced survival of rats injected with CRNK-16 leukemia cells in a dose-related manner. Acute administration of 2.5-3.5 g of ethanol/kg body weight, one hour before tumor inoculation, or chronic consumption of liquid diet containing ethanol for two weeks before and three weeks after tumor inoculation, significantly increased the number of lung metastases of MADB106 mammary adenocarcinoma. The ethanol-induced increase in the number of metastases was not correlated with plasma levels of corticosterone and was not altered by the opiate antagonist naltrexone. Incubation of spleen cells in vitro in the presence of ethanol, at concentrations comparable to those measured in the blood of ethanol-treated rats, significantly suppressed natural killer (NK) cell activity against MADB106 cells in a standard chromium-release assay and decreased the binding of effector to MADB106 tumor cells. However, neither acute nor chronic ethanol administration in vivo altered splenic NK activity against this tumor in the same in vitro assay, in which the ethanol would have been washed away. These results suggest that, in the presence of ethanol, tumor progression is facilitated. The possibility that this facilitation is related to ethanol-induced impairment of the normal tumoricidal interaction between NK and tumor cells is discussed.

Original languageAmerican English
Pages (from-to)74-86
Number of pages13
JournalBrain, Behavior, and Immunity
Issue number1
StatePublished - Mar 1992

Bibliographical note

Funding Information:
We thank Sin Boun, Berrilyn J. Branch, Erin Cody, Nick Lee, and David Pregerson for their careful assistance in running the experiments, Dr. Herbert Weiner for enriching discussions, and Dr. John C. Hiserodt for generously providing the CRNK-16 leukemia cells. Supported by NIAAA Grant AA 06744, the Veteran’s Administration Medical Research Service, and Trent and Mary Wells (A.N.T.), by NIH Grant NS07628 and a grant from the Bristol-Myers Squibb Company (J.C.L.), by Grant 038.1059 from the National Institute for Psychobiology in Israel (R.Y.), and by the UCLA Psychoneuroimmunology Program (R.Y. and S.B.-E.).


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