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Medical Research Centre, Prince Henry's Hospital St. Kilda Road, Melbourne, Victoria, Australia 3004
Abstract
The effect of differing degrees of destruction of the seminiferous epithelium on serum FSH levels and on Sertoli cell secretory function was studied in adult male rats. Germinal cell aplasia (Sertoli cell-only syndrome, SCO) was induced in male rats by fetal irradiation (250 rads) on day 20 of gestation. Destruction ofthe seminiferous epithelium was induced by treatment with either hydroxyurea (HU) or chronic feeding of a vitamin A-deficient diet (VAD).
Serum FSH, LH and testosterone were measured to assess pituitary-testicular interaction, and testicular androgen binding protein (ABP) was measured to evaluate Sertoli cell secretory function in these states. Serum LH was significantly elevated in all three treatment groups, while serum testosterone was significantly lower than normal only in SCO rats. The elevation of LH and the lowered testosterone levels suggest that there is partial Leydig cell failure in rats with germinal cell aplasia induced by fetal irradiation. Significantly elevated levels of serum FSH were seen in all three treatment groups; the degree of elevation was proportional to the severity ofthe induced testicular damage (normal adult males 378 ± 27, HU treated 751 ± 28, VAD 1019 ±49 and SCO rats 1070 ± 54 ng/ml, mean ± SEM).
Both the secretion rate of ABP as measured by its accumulation in the testis in the 16 h following efferent duct ligation, and the total amount of ABP both in testis and caput epididymis were markedly decreased in all three treatment groups in proportion to the severity of the induced testicular damage. These findings indicate that Sertoli cell secretory function was impaired as a result of the treatments used to induce testicular damage. The demonstration of impaired Sertoli cell secretory function in association with elevated serum FSH suggests that feedback regulation of FSH may be a function ofthe Sertoli cell.
Footnotes
Supported by the National Health and Medical Research Council of Australia and the Ford Foundation.
1 Presented in part at the 19th Annual Meeting ofthe Endocrine Society of Australia, August 18-20,1976 (1).
Received December 28, 1976.
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