The influence of hormonal treatment with beta-human chorionic gonadotropin for cryptorchidism on future fertility in rats

Abstract

There have been two treatment modalities for cryptorchidism such that surgical and hormonal; the latter being highly controversial. While some authors suggest that hormonal treatment increases the number and maturation of germ cells in cryptorchid testes, others believe just the opposite. We aimed to find out the sperm counts and testicular index; briefly fertility potential of the normally descended contralateral testes in adulthood period in rats treated with Beta-HCG in early period of their lives. Three groups, each including 10 rats aged 22 days old, in which delactation and normal feeding can be started, were formed to be Group 1: Sham operated, Group 2: Experimental cryptorchidism (EC) and Group 3: Hormone-treated after experimental cryptorchidism was performed (HT-EC). Left testis was placed in the abdomen in group 2 and 3. In group 1, a sham operation was performed. The rats in EC-HT group received subcutaneous injections of 50 IU/kg Beta-HCG daily for 7 days. Right orchidectomy was performed when they reached reproductive period to evaluate fertility potential with sperm counts and testicular index. Testicular index was calculated according to the formula "testicular length × width/weight of rat". Epididymal sperm count was made with hemocytometer. We evaluated the physical characteristics and fertility potential (sperm counts) of contralateral normal testes during adulthood in rats that underwent experimental unilateral cryptorchidism during infancy. A relationship between testis weight and sperm counts were also investigated. We could not find any direct correlation of sperm count with either testicular weight or testicular index in our study. Although the rats had normal testes at birth, we found decreased sperm counts in contralateral normal testes in EC group. This suggests that unilateral cryptorchidism may cause some systemic effects that reach the other testis. Hormone treatment was not beneficial. This is comparable to Nambirajan et al. who reported histological changes and decreased spermatogenic cell count in contralateral scrotal testes in experimentally induced unilateral cryptorchidism in early period of life in rats. Heiskanen et al. reported that treatment with Beta-HCG leads to decreased total sperm counts in the future due to increased germ cell apoptosis caused by hormonal withdrawal after treatment. Cortes et al. also reported decreased number of germ cells in 1-3 year-old boys who underwent surgery after unsuccessful Beta-HCG treatment. The reasons could be delayed testicular descent or adverse effect of hormone treatment though. Our results concurred with them. Apparently, our model has failed to mimic the pathophysiologic mechanisms of congenital cryptorchidism in humans. Furthermore, we applied hormone treatment in normal rats with normally descended testes. Therefore, the "by-product" information of our study is that, unnecessary use of Beta-HCG during infancy may impair future fertility. Our study suggests that Beta-HCG treatment may decrease sperm counts and decrease the future fertility potential. We could not find any direct correlation of sperm count with either testicular weight or testicular index.