The characteristic change in the distribution of S-100 immunoreactive folliculostellate cells in rat anterior pituitary upon long-term estrogen treatment is prevented by concomitant progesterone treatment.
The presence of folliculostellate cells in the anterior pituitary was described 49 years ago. These cells give about 10% of the whole cell population and through their long processes they provide intrahypophyseal communication. The folliculostellate cells contain S-100 protein. Its immunostaining was used to identify these cells. It was previously found that the diethylstilbestrol treatment basically influences the morphology and function of the trophic hormone secreting as well as the folliculostellate cells. In the present experiment, we have studied whether a concomitant progesterone treatment can prevent or attenuate changes caused by diethylstilbestrol treatment in the distribution of folliculostellate, prolactin, and GH cells. Diethylstilbestrol alone induced the appearance of prolactinomas. Inside the prolactinomas, folliculostellate cells were scattered but outside the prolactinomas they formed a demarcation line. Inside the prolactinomas, there were only a few growth hormone immunoreactive cells but they surrounded the prolactinomas in a ring-like pattern. When diethylstilbestrol was implanted with progesterone, the changes being characteristic for diethylstilbestrol treatment, could not develop. Concomitant progesterone influence prevented morphological changes in the anterior pituitary. Progesterone alone had no effect. In accordance with the formation of prolactinomas, the plasma prolactin level was very high in diethylstilbestrol treated rats. Concomitant progesterone treatment prevented the effect of diethylstilbestrol. Progesterone alone did not influence the prolactin level. GH levels did not significantly differ in any groups.
Heinzlmann
Andrea
A
Department of Human Morphology and Developmental Biology, Faculty of Medicine, Semmelweis University, Tuzoltó u. 58, Budapest 1094, Hungary.
Köves
Katalin
K
D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D004054:Diethylstilbestrol / Q000633:toxicity*; D004343:Drug Implants; D004347:Drug Interactions; D004968:Estrogens, Non-Steroidal / Q000633:toxicity*; D013006:Growth Hormone / Q000378:metabolism; D007150:Immunohistochemistry; D008297:Male; D010903:Pituitary Gland, Anterior / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D010911:Pituitary Neoplasms / Q000139:chemically induced / Q000473:pathology / Q000517:prevention & control*; D011374:Progesterone / Q000494:pharmacology*; D011388:Prolactin / Q000378:metabolism; D015175:Prolactinoma / Q000139:chemically induced / Q000473:pathology / Q000517:prevention & control*; D011863:Radioimmunoassay; D051381:Rats; D017207:Rats, Sprague-Dawley; D009418:S100 Proteins / Q000378:metabolism*
D015415:Biomarkers; D004343:Drug Implants; D004968:Estrogens, Non-Steroidal; D009418:S100 Proteins; D011374:Progesterone; D004054:Diethylstilbestrol; D011388:Prolactin; D013006:Growth Hormone