PROLACTIN BINDING TO 7,12-DIMETHYLBENZ(A)ANTHRACENE-INDUCED MAMMARY-TUMORS AND LIVER IN DIABETIC RATS

Abstract

Growth rates of 7,12-dimethylbenz(.alpha.)anthracene-induced mammary tumors and the specific 125l-labeled prolactin binding to membrane fractions prepared from livers and tumors were studied in rats made diabetic by streptozotocin injection. Growth was inhibited in a majority of tumors, and prolactin binding was reduced in tumors and livers from diabetic animals. Prolactin binding to individual tumors varied over a wide range in intact and diabetic animals. Scatchard analysis of binding data revealed that the apparent affinity of prolactin binding to liver and tumor membranes was similar (Ka .apprx. 3.0 .times. 109 M-1) and was not affected by diabetes. The reduction in prolactin binding to tumors may render these tissues less responsive to prolactin and explain the observed inhibition of tumor growth in diabetic rats. Some tumors in diabetic animals regressed despite relatively high levels of prolactin binding activity. Additional factors play important roles in the mechanism(s) by which the growth of 7,12-dimethylbenz(a)anthracene-induced tumors is impaired in the diabetic rat.