Inhibition of Testicular Androgen Biosynthesis by Treatment with LH-RH Agonists

It is well known that testicular function is controlled by hormones of the anterior pituitary gland. The absolute requirement for these hormones is demonstrated by the rapid atrophy of the sex accessory organs and inhibition of spermatogenesis following hypophysectomy (Wood and Simpson, 1961). The production of testicular steroids, in particular testosterone, is under the control of luteinizing hormone (LH), which is able to stimulate steroidogenesis in a variety of in vitro systems such as perfused testes, incubation of decapsulated testes, and suspensions of purified Leydig cells (Tsuhuhara et al,1977). There is good evidence showing that the action of LH in Leydig cells involves binding to specific receptors located on the plasma membrane, stimulation of cyclic AMP formation, and activation of protein kinase. The acute steroidogenic response of the testis to LH depends primarily on the activation of the enzymes controlling cholesterol side-chain cleavage, although there is also evidence for control mechanisms at a later step in the steroid biosynthetic pathway (Chasalow, 1979).