The mammary cancers which are rapidly induced by the oral administration of polycyclic aromatic hydrocarbons to rats are often hormone-dependent, and provide unique tools for the study of hormonal influences on tumor metabolism. The respiration of slices of these mammary tumors was quantitatively similar to that of the mammary gland of lactating rats; the high rates of anaerobic and aerobic glycolysis were typical of malignant tumors (157). The oxygen uptake of those mammary cancers having the histologic appearance of hormone-dependent neoplasms was decreased after ovariectomy. On the other hand, the respiration of the cancers which did not exhibit the histologic criteria of steroid-withdrawal atrophy was uninfluenced by excision of the ovaries. Administration of estradiol-17βto ovariectomized animals abolished the respiratory differences between the two types of tumor. Such endocrine treatments did not affect lactic acid formation under anaerobic or aerobic conditions.

Six pyridine nucleotide-linked dehydrogenases were determined in methylcholanthrene-induced mammary cancers and also in the rat mammary gland during pregnancy and lactation. The levels of these dehydrogenases formed characteristic patterns (157). The soluble DPN-linked malic dehydrogenase had the greatest activity in normal hyperplastic mammary gland, while lactic dehydrogenase was the most active enzyme in the mammary cancers (and in some transplantable rat tumors). The levels of the TPN-specific "malic enzyme" were very low in the induced mammary carcinomata. Pronounced endocrine effects were observed on the dehydrogenase activities of the mammary cancers. The most striking change was an 11-fold increase in the levels of "malic enzyme" in the cancers of ovariectomized animals treated with large doses of estradiol-17β, a procedure which caused vast accumulation of lipids in the epithelial cells of some of these tumors. The activity of lactic dehydrogenase correlated well with progression or regression of the cancers brought about by modification of the hormonal status.