Abstract
Pure ethanol in experimental animal studies, may not primarily be carcinogenic, but secondarily it can act chemically and synergistically as a co-carcinogen via its endogenous metabolites and associated dietary and exogenous factors. However, ethanol, being a small molecule and miscible with water and most lipids, can readily enter cell membranes and directly affect cell function. In an in vitro study where ethanol was added to the culture medium for Lewis lung carcinoma, a dose-dependent suppression of tumour growth occurred. In the in vivo study, sequestration of the Lewis lung carcinoma in the lungs followed tail-vein injection in C57BL/6 mice. Starting on the second day after tumour implantation, primary pulmonary exposure was carried out with inhalations of 0.4% ethanol vapour from an aerosol for 70 min daily, this was continued for 17 days. This resulted in a marked reduction of the pulmonary tumour growth. Exposure to 0.1% ethanol vapour did not significantly affect the growth of Lewis lung carcinoma tumour. The optimum ethanol aerosol applications may thus be tumoricidal. Whether any ethanol secondary metabolites are involved is as yet uncertain.
Key words: Lewis lung carcinoma, Ethanol vapour, Tumour growth retardation
Footnotes
Supported by the Leahi Foundation, American Lung Association of Hawaii
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