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SUMMARY
Medium from cultures of mature rat seminiferous tubules contained a substance which suppressed, in a dose-related manner, the luteinizing hormone releasing hormone (LH-RH)-stimulated secretion of FSH by cultured rat pituitary cells. The secretion of LH was suppressed to a lesser extent and the basal secretion of both LH and FSH was inconsistently affected. Gel filtration on Sephadex G-100 did not fractionate the activity. The active material did not inhibit the secretion of TSH or destroy LH-RH and the activity was not due to testosterone or oestradiol in the medium. Control media from liver cultures were inactive. It is concluded that inhibin is present in media from cultures of rat seminiferous tubules.
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A bioassay for inhibin based on the suppression of gonadotrophin releasing hormone (Gn-RH)-stimulated secretion of FSH by primary monolayer cultures of rat anterior pituitary cells is described. The cultures were exposed to standard or test materials for 3 days. The levels of FSH in the media were measured by radioimmunoassay after exposure for 6 h to a maximally stimulating concentration of Gn-RH (10 nmol/l). The standard was prepared from ovine testicular lymph. Several preparations of proteins from gonadal tissues or secretions suppressed the levels of FSH in parallel with the standard. The levels of LH were also reduced but higher doses of active material were required. Non-specificity from cell damage and inactivation of Gn-RH have been excluded. The secretion of gonadotrophins by the pituitary cells was also inhibited by androgens, but not in parallel with the standard and secretion of LH was affected more than that of FSH. Control lymph protein preparations from castrated sheep had no detectable activity. The assay was sensitive and had adequate precision and practicability. It has proved useful for monitoring preliminary steps in the purification of inhibin.
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Pharmacological doses of glucocorticoids inhibit thyroid function in man and laboratory animals due to suppression of thyrotrophin (TSH) secretion (Wilber & Utiger, 1969). Administration of prednisolone or dexamethasone for 1–2 days results in a suppression of basal serum TSH levels in normal subjects and in patients with primary hypothyroidism, whilst the pituitary TSH reserve capacity, as assessed by the response to synthetic thyrotrophin releasing hormone (TRH), remains unaltered (Wilber & Utiger, 1969; Besser, Ratcliffe, Kilborn, Ormston & Hall, 1971; Haigler, Pittman & Hershman, 1971). However, impairment of serum TSH response to administered TRH does occur in patients treated with glucocorticoids for 1 or more months (Otsuki, Dakoda & Baba, 1973). These studies suggest that glucocorticoids may inhibit TSH secretion at both hypothalamic and pituitary levels but the main effect of the short-term treatment is suppression of TRH production.
Nicoloff, Fisher & Appleman (1970) found that the circadian rhythm of thyroidal
