Pathophysiological changes associated with the exposure of sustained delivery of glucocorticoids on pituitary adenoma cell line.

摘要

Glucocorticoid receptor rich tissues such as pituitary cells express tissue specific 11 beta hydroxysteroid type 1 enzyme, which causes cortisol to act as an autocrine, anti-proliferative, pro-differentiation stimulus in normal tissue. In pituitary tumor cells there is a strong correlation indicating a shift from 11 beta hydroxysteroid type 1 enzyme activity to 11 beta hydroxysteroid type 2 enzyme activity. This shift causes an anti-proliferative effect, which may be effective in suppressing tumor activity. Overall, the results indicated a decreased in cell number for both acute and chronic administration over a 96 hour period without inducing cellular damage (MDA), reactive nitric intermediates (nitric oxide) or reducing cellular antioxidant status (glutathione). Cortisol administration cause an increase in the number of hyperchromic nuclei suggesting cell cycle regulation. These findings conclude that cortisol administration to pituitary tumor cells may offer a future means of treatment for hypophysectomized patients.