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Plasma FSH and LI-I were determined by radioimmunoassay on six normozoospermic men, twelve oligozoospennic (sperm concentration less than 40×10[6]/ml) and thirty-four azoospermic. Klinefeter's syndrome and obstructive azoospermia were excluded from this study. Plasma FSH of the azoospermic group (18.1mIU/ml) was sigificantly higher than that of the normozo-oligozoospermic group (11.1mIU /ml). Azoospermic men having no germ cells on testicular biopsy showed plasma FSH as high as 21.0 mIU/ml. Those having germ cells, however, showed no significant increase of FSH compared with the normozo-oligozoospennic group. There was no correlation between testicular biopsy score count and plasma FSH. Plasma LH of the azoospermic men without germ cells on testicular histology was 27.6 mIU/ml which was significantly higher than that of the normozo-oligozoospermic group (18.2mIU/ml). Plasma LH of the azoospermic men without germ cells showed positive correlation with their plasma FSH. From the above results, it might be suggested that FSH inhibiting factor originating from the germ cells probably gives suppression on production of FSH whereas androgen on release of FSH.

1. Normal testes of the adult rat and man were ele c tron microscopically observed. Seminoma, teratoma, and embryonal carcinoma were also studied with electron micrographs. 2. As to spermatogenesis, formation of the acrosome in the rat spermatid was demonstrated as well as the structure of the axial fiber bundle which was seen composed of the tubular arrangement of nine axial filaments enveloped with the mitochondrial helix. The mitochondria of the helix were of tubular appearance, being devoid of the mitochondrial cristae but having thick limiting membrane (Fig. 1-4). 3. In general, germ cells were abundant in t he mitochondria and rough surfaced endoplasmic reticulum, but no lipid droplet was found in the cytoplasm. The nuclei were finely granular and of high electron density (Fig. 1, 2, 7, 9, 10). 4. Both Sertoli and Leydig cells were rich in lipid d roplets which are known to be related with steroid production. Lipid droplets in Leydig cell showed two different forms, one was globular and another course granular (Fig. 12). 5. Sertoli cells were small and polygonal in shape, the cytoplasm of which was less dense comparing with germ cells. Cytoplasmic organellae were rather scant. They made network or syncitium with indistinct cytoplasmic border. Leydig cell had vesicular cytoplasm due to vacuoles, some of which contained finely granular substance (Fig. 5, 6, 8, 10). 6. Testicular tumor cells had large nuclei with hypertrophied nucleoli, the nu c leolonema of which were quite prominent. The nucleus of seminoma cell was electron dense with fine granules, whereas that of teratoma was less dense. In embryonal carcinoma the nucleus showed aggregation of course granules arranged in reticular fashion. There were a few interesting findings as to nuclei of the testicular tumor cells. In seminoma, the outer layer of the nuclear membrane was partly detached and protruded into the cytoplasm. In teratoma, "nuclear extrusion" was observed . This phenomenon is, probably, a result of activ e movement of nuclear substance to the cytoplasm. In embryonal carcinoma, osmiophilic substance, RNA from Pars amorpha of the nucleolus, was present close to the nuclear membrane. In cytoplasm of those tumor cells, mitochondria and endoplasmic reticulum were not abundant (Fig. 13-18).

To examine the changes occurring in the testis in the rebound phenomenon, adult male Wistar rats were treated with 0.3 mg of testosterone propionate (TP) daily for 39 days. Observations were made at 0, 13, 26, 52 and 78 days following the TP treatment. The response of the testis was investigated histologically and was also analyzed using the tissue kinetic technique. No obvious changes in body weight observed but the testicular weight of the TP treated rats was half that of the control testis by the time TP treatment was terminated. However, from that time onward, the testicular weight started to increase. By the 78th day it was heavier than that of control. The weight responses of the seminal vesicle and prostate were just the reverse of that displayed by the testicle. The histological changes in TP treated rats were as follows: Soon after treatment, the diameter of the seminiferous tubule decreased and the spermatids were either absent or present in small numbers. No histological changes were seen in the seminiferous epithelium and Sertoli cells in themselves. The interstitial tissue was atrophic. The test group recovered from any TP induced changes, that is, there were no histological differences between the group on the 78th day after treatment and the control group. Spermatogenesis was measured by determining the relative number of germ cells in round tubular cross sections at stage VII of the seminiferous epithelium cycle. The relative number of type A spermatogonia and preleptotene spermatocytes remained similar to the control value in rats with maximal testicular atrophy due to TP treatment. When the TP injections were terminated, the relative numbers of pachytene spermatocytes and step 7 spermatids were 70% and 51 % of the control group, respectively. However, 78 days after TP treatment, the relative number of pachytene spermatocytes and step 7 spermatids were 120% and 160% of the control group, respectively. These changes demonstrate the "rebound phenomenon". Autoradiographic study using 3H-thymidine revealed that there was no great difference in the duration of seminiferous epithelium cycle between the TP treated group and control group. There was a slight distribution of the most advanced cells when the TP injections ended. In order to conclude that there were definite changes in the duration o[ the spermatogenesis, it is necessary to conduct a more precise experiment. It can be concluded from these observations that TP injection to adult male Wistar rats induced the "rebound phenomenon"; the most remarkable changes were seen in the relative number of pachytene spermatocytes and spermatids.

Oxygen toxicity problem has been much discussed but real causative factors are still unknown. Histological and cytochemical studies on effects of oxygen under ambient prossure, 3.5 ATA. abs., with Wistar strain male rats, focused on changes of gonadotropic organs, were accomplished. Results were as follows. Premature young rats were more influenced by pure oxygen than adult group and ensured physical retardation. Reduced succinylcholine dehydrogenase activities were observed in both kidneys and testes after a series of intermittent exposure to OHP. However, histological changes were little except emphysematous lungs by autopsies. Some possibilities are discussed in this article that hypoplasia of testicular germ cells would be caused by vas constrictive effect at increased pO2 environment.

The rabbit testes were exposed to the active anaphylaxis with the bovine erythrocyte as antigen and the reverse anaphylaxis with the anti-rabbit erythrocyte sera of the guinea pig. Allergic orchitis ensued, the main findings of which were vascular and hemorrhagic changes. Spermatogenesis was markedly damaged, and there were degeneration of germ cells and appearance of giant cells. The follow-up study showed that changes in the seminiferous tubuli were still progressive without regeneration even at the time when the stroma was already toward regeneration. From the experimental results and the study of Part 1, the relation between mumps orchitis and spermatogenic failure was discussed.