Abstract
In mammals spermatogenesis is totally dependent upon testosterone. It is produced by the Leydig cells and acts upon the Sertoli and peritubular cells of the seminiferous tubule and, via processes which are virtually unknown, drives spermatogenesis (Sharpe, 1986). There has been a long-running debate about how much testosterone is needed to maintain spermatogenesis and recent developments suggest that current concepts may require modification. There are many studies in the literature which show that spermatogenesis can be 'maintained' by exogenous testosterone in hypophysectomized rats or in stalk-sectioned monkeys when the intratesticular level of testosterone is only 10–20% of normal (e.g. Boccabella, 1963; Buhl, Cornette, Kirton & Yaun, 1982; Marshall, Wickings, Ludecke & Nieschlag, 1984). However, it is clear that maintenance is only qualitative and that subnormal numbers of sperm would be produced in these situations, and these may suffer from subtle defects while appearing morphologically normal (Huang & Nieschlag, 1984). To

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