The thymic factor tactivin prevents ACTH from stimulating steroidogenesis by mouse adrenal cells.

The effect of tactivin, a thymic hormonal factor, (MW 1-6 KD), on the adrenal glucocorticoid function in mice was studied. Tactivin (0.1-2 micrograms/mouse i.p.) produced a slight decrease in plasma corticosterone. The decrease was much more pronounced when tactivin was administered to mice with a high basal level of the hormone. The tactivin supplement had a significant suppressive effect on corticosterone production in both the whole adrenals and the intact isolated adrenal cells. When added at the doses of 0.00064-2 micrograms/ml to the isolated adrenal cells in the presence of ACTH, tactivin abolished the stimulatory effect of corticotropin on corticosterone production. The abolition was complete at a low dose (1.6 microIU/ml) and incomplete, yet significant, at a high dose of ACTH (1600 microIU/ml). The in vitro data are in a good agreement with those obtained in the in vivo experiments. The stimulatory effect of a synthetic analog of cAMP-Dibutyryl-cAMP on the steroidogenesis of adrenal cells was as pronounced as that of ACTH. Nevertheless, tactivin exerted no influence on Bu2-cAMP stimulation. The results indicate that tactivin prevents ACTH from acting on steroidogenesis at some time point preceding the formation of secondary messengers.