Endocrine Abstracts

The endocrine disruptor compounds (EDC) (e.g. chlorobenzenes (ClB), phenurone (PU), monurone (MU), diurone (DU)) are accumulative, lipophilic, chemical pollutants that can disturb the homeostatic balance and exert tumorigenic effects. The aim of the present study was to investigate the effects of EDCs on the adrenocorticotropic hormone (ACTH) and prolactin (Prl) release in primary cell cultures derived from rat normal adenohypophysis and prolactinoma.

The prolactinoma formation was induced by estrone-acetate (2 mg/bw kg/day; subcutan for 6 months). The ten-day-old cell cultures, obtained from rat normal adenohypophysis and prolactinoma, were treated as follows: I. 0.1 μg/ml EDCs (ClB, MU, DU, PU) for 1 hour; II. 10 μg/ml arginine-vasopressine (AVP) for 1 hour in itself and subsequently 10 μg/ml corticosterone was also added; III. EDCs in combinations with AVP and corticosterone. ACTH and Prl levels were detected in supernatant media by radioimmunoassay. The protein content was measured by Protein Assay system.

The basal ACTH (1500 pg ACTH/mg protein) and Prl (7 ng Prl/mg protein) levels did not change significantly after the EDC treatment in the supernatant media of the adenohypophysis cell culture. The EDCs (ClB:14500; PU:11900; MU:13100; DU:13800 pg ACTH/mg protein) significantly increased the AVP induced ACTH release of normal adenohypophyseal cells (10200 pg ACTH/mg protein) but did not influence the effects of corticosterone. The prolactinoma cells showed increased secretions of ACTH (2200 pg ACTH/mg protein) and Prl (17,2 ng Prl/mg protein) compared with the normal adenohypophyseal cells. The basal ACTH and Prl levels in the supernatant media of the prolactinoma cells were significantly increased by the EDC treatments (ClB:2973; PU:2417; MU:2539; DU:2701 pg ACTH/mg protein; ClB:23.1; PU: 19.7; MU:21.5; DU:22.4 ng Prl/mg protein).

The ACTH and Prl synthesis and release capacity of normal adenohypophyseal and prolactinoma cells were altered by EDCs. This work was supported by: TAMOP 4.2.1/B-09/1/KONV-2010-0005; HURO/0901/037/2.2.2.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This work was supported, however funding details unavailable.