Effects of Estradici and Tamoxifen on Creatine Kinase in Rodent Mammary Carcinomas1

The effects of altered estrogenic environments on creatine kinase (CK) and adenylate kinase (AK) were studied in two rodent mammary tumor systems, R3230AC and primary 7,12-dimethylbenz(a)anthracene iDMB \) indim-d carcinomas, to determine whether response of these enzymes could be related to their hormone dependence. The hormonal perturbations studied were ovariectomy and administration of various doses of estradici valerate or the antiestrogen tamoxifen. Total CK activity and AK activity were assessed by a spectrophotometric assay followed by electrophoretic separation of the CK isozymes to determine their relative activities. In the ovarian-independent R3230AC tumors, estrogen treatment produced a dose-related decrease in CK activity, whereas CK was not responsive in ovarian-dependent DMBA-induced tumors. Adenylate kinase activity remained unchanged regardless of the hormonal perturbation. Glucose-6-phosphate dehydrogenase and lactate dehydrogenase, which were studied for comparative purposes, were both estrogen responsive. While both estrogenic and antiesrrogenic effects on enzyme activities were observed in the DMBA-induced tumors, the effect of tamoxifen in the R3230AC tumors was generally estrogenic. We conclude that the effect of estrogen on CK-BB in DMBA-induced tumors is not sufficient to be used as a biochemical marker of hormone depen dence.