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Seasonal variation in specific plasma- and target-tissue binding of androgens, relative to plasma steroid levels, in the brown trout, Salmo trutta L.

Pottinger, T.G.. 1988 Seasonal variation in specific plasma- and target-tissue binding of androgens, relative to plasma steroid levels, in the brown trout, Salmo trutta L. General and Comparative Endocrinology, 70 (2). 334-344. 10.1016/0016-6480(88)90153-0

Abstract
The circulating levels of the plasma androgens, testosterone and 11-ketotestosterone, and their specific binding to skin cytosol, skin nuclear extract, and plasma were determined in mature male and immature male and female brown trout during a single spawning cycle. 11-Ketotestosterone was not bound by any of the fractions examined whereas testosterone was bound with high affinity to plasma (kD = 32.6 nM), skin cytosol (kD = 16.9 nM), and skin nuclear extract (kD = 2.6 nM). The binding capacity of each fraction varied independently with time. In mature male fish an increase in specific binding of testosterone to nuclear extract, from 77 to 269 fmol/mg protein, occurred between September and November, coincident with peak androgen levels. Following the spawning period and the decline in androgen levels, nuclear-binding capacity in mature fish dropped to a level similar to that of immature fish by June. Nuclear binding in immature fish remained in the range 25–75 fmol/mg protein throughout. Plasma-binding capacity of both mature and immature fish declined during the spawning period, from 190 to 125 nM in mature fish and from 360 to 125 nM in immature fish. Plasma-binding capacity in both mature and immature fish increased following spawning to reach levels of 340 nM (mature) and 250 nM (immature). Little change was observed in cytosol-binding capacity of either mature or immature fish. The results suggest that androgen-induced structural changes in the integument are predominantly testosterone stimulated, are initiated by an increase in the concentration of a specific testosterone-binding protein within the nucleus, may be potentiated by a drop in plasma testosterone-binding capacity, and that a cytosol-binding protein of intermediate affinity for testosterone may maintain a high intracellular concentration of steroid.
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