Assessment of the ratio of live to dead spermatozoa showed that the ultimate loss of fertilizing capacity by the spermatozoa in both intact and gonadectomized males was not at first due to an increased incidence of dead spermatozoa in the epididymis, though progressively more dead and degenerated spermatozoa were gradually to be seen in the samples.The fertilizing capacity of the spermatozoa was lost more rapidly (within 8 days) in gonadectomized animals if they were also hypophysectomized. Administration of HCG to these animals failed to maintain normal viability in the spermatozoa.A gradual decrease in the occurrence of 'light' cells in the lining tissue of the duct is reported, following gonadectomy.It is concluded that circulating androgen is unquestionably required for the normal survival of spermatozoa in the tail of the hamster epididymis and that it probably achieves its effect through its influence on the epididymal epithelium. The findings are discussed in relation to the general hormonal control of sperm survival in the epididymis.
SUMMARY The effects of testosterone, dihydrotestosterone, 3α- and 3β-androstanediol on the fertilizing capacity of mature epididymal spermatozoa and on the production of fructose by the seminal vesicles were compared in golden hamsters. When injected subcutaneously into castrated animals, 100 μg testosterone, 75 μg dihydrotestosterone but only 12·5 μg 3α-androstanediol per day were required to maintain the fertilizing capacity at the control level for 12 days; 3β-androstanediol failed to maintain the fertilizing capacity of epididymal spermatozoa for 12 days. Although testosterone and dihydrotestosterone were equipotent in stimulating production of fructose by the seminal vesicles, 3α- and 3β-androstanediol were much less effective. The discrepancy in the response of the cauda epididymidis and seminal vesicles to 3α-androstanediol suggests that the hormonal requirements for sperm survival in the cauda epididymidis differ from those for the production of fructose in seminal vesicles. The results suggest that circulating testosterone may be relatively inactive in the cauda epididymidis and that the maintenance of fertilizing capacity of epididymal spermatozoa might be correlated with the reduction of dihydrotestosterone to the more potent androgen 3α-androstanediol by mature spermatozoa.
SUMMARY The effect of progesterone on the maturation and viability of epididymal spermatozoa was tested in golden hamsters. The corpus epididymidis and ductus deferens were unilaterally ligated so that mature spermatozoa were isolated in the left cauda epididymidis whilst the contralateral epididymis was left intact. Fertility trials showed that after eight daily consecutive injections of progesterone (1·0 mg) spermatozoa on both sides retained normal fertilizing ability. Treatment with progesterone (0·25 and 1·0 mg) for 12 days, however, decreased the fertilization rate of retained spermatozoa to 44·4% and 0%, respectively, whereas fertilizing ability of spermatozoa from the intact cauda epididymidis remained unimpaired. In addition, progesterone (1·0 mg/day) did not influence passage of spermatozoa through the epididymis. Male hamsters treated with progesterone (0·25 mg/day) in combination with testosterone, 5α-dihydrotestosterone (5α-DHT) or 3α-androstanediol (all at 50 μg/day for 12 days revealed that 3α-androstanediol and 5α-DHT (but not testosterone) antagonized the antifertility effect of progesterone on retained epididymal spermatozoa. Furthermore, treatment of castrated hamsters with testosterone, 5α-DHT or 3α-androstanediol (100, 75 and 12·5 μg/day, respectively) in combination with progesterone (1·0 mg/day) showed that progesterone inhibited the stimulatory effect of testosterone but not that of 5α-DHT and 3α-androstanediol. The dissimilar effect of progesterone on fertilizing ability of spermatozoa in ligated and intact epididymides is discussed.
Fertile male hamsters were injected daily with 66 mg \g=a\-chlorohydrin/kg to determine the onset and duration of infertility. None of the males became infertile within the first 2 days but marked loss of fertilizing ability of spermatozoa had occurred by 24 hr from the second injection. Infertility occurred in all five males after the fourth dose. The fertilizing ability of the spermatozoa was not impaired when the equivalent of four daily doses was given as a single dose, thus indicating that sequential daily treatment was necessary for the induction of infertility. The prompt recovery of fertilizing ability of spermatozoa in males which had ligated ductuli efferentes and were given four daily doses of\g=a\-chlorohydrin (66 mg/kg) shows that transport of epididymal spermatozoa and their acquisition of fertilizing ability are not influenced by the drug.
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