Is there any association between the pharmacologic control of prolactin release and its action on mammary carcinogenesis in the rat?
Pretreatment of female Wistar rats with various compounds (coumarin, 4-methyl-phenobarbital, carbon tetrachloride) on mammary tumour production by 7,12-dimethylbenz(a)anthracene (DMBA) has been studied. The test compounds brought about a variety of actions on DMBA tumours; their effect varied from none (phenobarbital, carbon tetrachloride) to decreased incidence and delayed appearance (coumarin, 4-methylcoumarin). In all cases studied increased prolactin level was found. The inhibitory action of coumarin on tumour incidence and multiplicity showed a dose-related association with elevated serum prolactin and reduced hepatic drug metabolism. These results indicate that the production of DMBA-induced mammary adenocarcinomas in the rat is not associated with serum levels of prolactin. Our results suggest that in this model for tumorigenesis, prolactin only plays the role of a promoter after the carcinogenic event.
D015127:9,10-Dimethyl-1,2-benzanthracene; D000818:Animals; D002251:Carbon Tetrachloride / Q000494:pharmacology; D003374:Coumarins / Q000494:pharmacology; D005260:Female; D008325:Mammary Neoplasms, Experimental / Q000097:blood / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology*; D010634:Phenobarbital / Q000494:pharmacology; D011388:Prolactin / Q000378:metabolism* / Q000502:physiology; D051381:Rats
D003374:Coumarins; D015127:9,10-Dimethyl-1,2-benzanthracene; D011388:Prolactin; D002251:Carbon Tetrachloride; D010634:Phenobarbital