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Ethanol was administered to mice either by repeated intraperitoneal injection, or orally in the drinking water over an extended period of time. Following intraperitoneal ethanol pre-treatment further groups of mice received an injection of benzo(a)pyrene. Alcohol intake decreased the level of microsomal aryl hydrocarbon hydroxylase which corresponded to the observed decrease in DNA binding of benzo(a)pyrene. In contrast, the number of tumors which developed in the alcohol pre-treated mice exceeded those of the control animals.

The effect of chronic ethanol intake on the growth and spread of some murine tumors has been investigated. The treatment had no effect on the B 16 melanoma but tended to decrease the number of Ehrlich ascites cells. In the case of the Lewis lung carcinoma, administration of ethanol for two weeks tended to lower the number of metastases to the lung without significantly affecting the primary tumor size, whereas more prolonged ethanol intake decreased the weight of the primary tumor in addition to decreasing its dissemination.

The plasma obtained from fed and starved lean, normal and obese women was estimated, by a radio-immunoassay method, for prostaglandins, owing to their implication in the regulation of adipose tissue lipolysis and the development of obesity. No significant differences were found due to nutritional status or body-build. However, a significantly higher plasma concentration of prostaglandins of the E-type than of the F-type, was found consistently. The very low levels of prostaglandins observed (a range of 0.10--0.15 ng ml-1 for E-type and a range of 0.05--0.07 ng ml-1 for the F-type) may be due, in part, to the activity of a plasmatic prostaglandin metabolizing system.