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Influence of Diethylstilbestrol Treatment on Prolactin Cells of Female ACI and Sprague-Dawley Rats¹

Medical Department, Brookhaven National Laboratory,³ Upton, New York 11973

In a comparative study, female ACI and Sprague-Dawley rats were implanted with pellets containing 5 mg diethylstilbestrol (DES) and 15 mg cholesterol for periods ranging from 2 to 214 days. Strain differences in mammary tumorigenesis, plasma prolactin levels, and gross pituitary responses indicated a desirability for examining the cytology of pituitary glands that were fixed during the course of this study and an immunohistochemical evaluation of their prolactin cell responses. Although plasma prolactin levels were elevated in both strains by 2 days after DES pellet implantation, during the first 10 days of treatment there were no significant increases in pituitary weight in both strains. Pituitary glands from experimental animals of both strains killed on Day 10 exhibited enlarged anti-rat prolactin-binding cells. By Day 28, the pituitary glands of DES-treated ACI rats were significantly enlarged, and a hypertrophic and hyperplastic response of their prolactin cells was detected. From Day 56 to the end of the experiment, gross pituitary tumorigenesis was evident in the ACI but not in the Sprague-Dawley rats. At the microscopic level, adenomatous lesions involving prolactin cell hyperplasia were observed in both strains. Sprague-Dawley and ACI rats exhibited multiple centers of marked vascularization predominated by granular acidophilic cells. These centers were more extensive and larger in the pituitaries of the ACI rats. Two types of immunoreactive prolactin cells were observed in lesioned pituitary glands of both strains: polyhedral, strongly reactive cells which were hypertrophic and more numerous in the ACI rats; and smaller, weakly reactive cells which were numerous in the adenomatous areas of the glands in both strains. It was concluded that the lesions in ACI and Sprague-Dawley females represented different quantitative responses of their prolactin cells to DES treatment.

¹ Research performed under United States Department of Energy Contract EY-76-C-02-0016, National Cancer Institute Contract Y01-CP-30213, and USPHS Grant 5-T01-Ca-05243.

² To whom requests for reprints should be addressed.

³ Operated by Associated Universities, Inc., under contract to the United States Department of Energy.

Received 8/18/78. Accepted 11/28/78.

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