AN INVESTIGATION OF THE DECREASE IN THE METABOLISM OF HEXOBARBITAL, AMINOPYRINE AND p-NITROBENZOIC ACID BY LIVER FROM RATS BEARING A PITUITARY MAMMOTROPIC TUMOR

¹ Section of Endocrinology, Reproduction Research Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland

The effects of liver cell hypertrophy, adrenalectomy and castration on the metabolism of hexobarbital and the production of formaldehyde from aminopyrine were studied in liver from control and mammotropic tumor (MtT)-bearing male rats. There was no decrease in some liver constituents (dry weight, deoxyribonucleic acid or microsomal protein and nitrogen) from tumor-bearing rats as compared with control animals. A decrease in one or several of these liver constituents may have been expected if liver cell hypertrophy without, for example, a concomitant increase in microsomal protein were present in MtT-bearing rats. The metabolism of hexobarbital and the formation of formaldehyde from aminopyrine by the liver 9000 x g supernatant fraction were decreased in MtT rats as compared with control rats regardless of the liver constituent used to express this metabolism. Hexobarbital sleeping time was increased in tumor-bearing rats. Inhibitors of the in vitro hepatic metabolism of hexobarbital or aminopyrine were not found in tumor, serum or liver from MtT rats. Growth of the MtT in adrenalectomized and/or castrated male rats produced a decrease in the hepatic metabolism of hexobarbital, aminopyrine and p-nitrobenzoic acid similar to that found in liver from unoperated tumor-bearing animals. Anterior pituitary hormones (corticotropin, somatotropin and prolactin) secreted by this MtT in rats may have decreased the hepatic microsomal metabolism of some compounds by acting directly on the liver in vivo.