The general hormonal requirements for the restoration of spermatogenesis in regressed hypophysectomized rats were investigated. With the aid of the Staput fractionation technique, it was established that thymidine-3H was readily incorporated into spermatogonia and resting spermatocytes. Labeled cells did not progress to form appreciable numbers of primary spermatocytes or spermatids in the absence of hormonal replacement. The inhibition of formation of pachytene primary spermatocytes in hypophysectomized rats was overcome by administration of follicle-stimulating hormone (FSH), luteinizing hormone (LH), or testosterone, but a combination of either FSH plus LH, or FSH plus testosterone, was required for the progression of pachytene primary spermatocytes to spermatids and spermatozoa. Carnitine acetyltransferase (CAT) measurements in testes from various groups of animals provided ancillary evidence consistent with the conclusion that either FSH, LH, or testosterone was required for the normal restoration of pachytene-diplotene spermatocyte formation. However, one or more additional blocks in spermatogenesis existed in hypophysectomized animals, since elevation of depressed testicular CAT levels in hypophysectomized rats to normal levels required FSH plus LH, or FSH plus testosterone. Cortisone and thyroxin treatment had no measurable effects on testicular function in hypophysectomized rats.
The Distribution of Carnitine, Acetylcarnitine, and Carnitine Acetyltransferase in Rat Tissues
