Enucleation for prepubertal leydig cell tumor

PURPOSE: Leydig cell tumors in children are rare, comprising only 4% to 9% of all primary testis tumors in prepubertal males. Almost all of these boys present with isosexual precocious pseudopuberty associated with increased testosterone, low gonadotropin levels and a testis mass. We present our experience with testis sparing enucleation of Leydig cell tumor in prepubertal boys. MATERIALS AND METHODS: Two patients presented with isosexual precocious puberty at ages 6 and 9 years. Each patient had a well circumscribed, painless testicular mass, increased serum testosterone (101 and 444 ng/dl [normal 0 to 25]), normal gonadotropins and negative alpha-fetoprotein levels. Both patients underwent successful enucleation of the testis mass following proper testis oncological surgical principles. RESULTS: Both patients had normalization of the serum testosterone following enucleation of the Leydig cell tumor. At 9 and 44 months of followup they have maintained normal ipsilateral testicular volume compared to the contralateral gonad, and 1 patient entered puberty spontaneously at 1 year postoperatively. Neither patient suffered any morbidity, and both have presumably benefited from preservation of the involved gonad with preserved testicular volume. CONCLUSIONS: Prepubertal boys with isosexual precocious pseudopuberty, an isolated testis mass, increased testosterone and low or normal gonadotropin levels can reliably be diagnosed with Leydig cell tumors. Based on the ability to establish the diagnosis preoperatively and the universal benign behavior of unilateral, prepubertal Leydig cell tumor, we believe these patients are best treated with testis sparing enucleation of the tumor. In view of the high likelihood that this tumor in prepubertal boys is benign, a transscrotal surgical approach should be considered.     

Dose and time related responses of the irradiated prepubertal rat testis

The testes of prepubertal rats were locally irradiated with 300 kVp x-rays to doses of between 1 and 15 Gy. Leydig cell function was assessed between 2 and 36 weeks post-irradiation. Dysfunction was observed at two weeks as evidenced by a reduction in serum levels of testosterone to between 40 and 70% of control, with a threshold dose of about 5 Gy. Endocrine deficiencies in the Leydig cell population were indicated at later times by increased serum levels of LH, although serum testosterone concentrations recovered to control levels. The elevations in serum LH increased with time suggesting progressive Leydig cell failure.     

Intratesticular factors and testosterone secretion: The effect of treatment with ethane dimethanesulphonate (EDS) and the induction of seminiferous tubule damage

The role of seminiferous tubule dysfunction in regulating the levels of a factor (or factors) in testicular interstitial fluid (IF) which stimulates Leydig cell testosterone secretion in vitro, was assessed by injecting rats with the Leydig cell toxin, EDS. Within 72 h of treatment EDS destroyed the Leydig cells and concomitantly reduced IF testosterone to undetectable levels. This was associated with nearly a 2-fold increase (P less than 0.001) in levels of the IF-factor(s) as judged by the enhancement of hCG-stimulated testosterone production (= IF bioactivity). By 3 weeks, and thereafter up to 10 weeks post-EDS, Leydig cells regenerated within the testis, and testosterone levels returned to control values, but IF-bioactivity remained significantly increased. The latter was associated with seminiferous tubule dysfunction as indicated initially by testicular morphology, raised serum levels of FSH and reduced testicular weight. For animals with normal testosterone levels, there was a significant negative correlation (r = -0.57, N = 46; P less than 0.001) between testicular weight and IF bioactivity. A similar increase in IF bioactivity in the presence of normal testosterone levels was observed in rats in which patchy severe seminiferous tubule damage had been induced by short-term cryptorchidism. It is concluded that, in addition to testosterone, seminiferous tubule function may dictate the intratesticular levels of the testosterone-stimulating factor(s) in IF.     

Testicular LH receptors during aging in Fisher 344 rats

Levels of serum LH, prolactin, testosterone, progesterone and 17-OH progesterone and the testicular concentration and total content of LH receptors were measured in 4-, 11-, 18-, and 27-month-old Fisher 344 rats. All 27-month-old rats had Leydig cell tumors. At first, testicular LH receptor levels decreased with age, but with the appearance of the testicular tumors, these levels increased dramatically. Serum prolactin levels fluctuated with age, but were significantly decreased in 27-month-old rats, as were serum LH levels. Serum testosterone levels decreased steadily with age, while the testosterone-LH receptor ratio remained constant until the appearance of the testicular tumors, after which the ratio decreased precipitously. Serum progesterone levels remained constant throughout the life of Fisher 344 rats until the appearance of testicular tumors, when they increased dramatically. Serum 17-OH progesterone levels were increased significantly at 11 and 27 months as compared to four months of age, but levels at 18 months were similar to those seen in the 4-month-old animals. Therefore, in aged Fisher 344 rats with spontaneous Leydig cell tumors, there is an alteration in the testicular testosterone synthesizing pathway at a step after progesterone.     

Leydig Cell Function in Rats Chronically Deprived of Normal Gonadotrophic Stimulation: The Effect of Treatment with hCG

Leydig cell function was assessed in adult rats 11 months after active immunization against LH-RH. Immunized rats were divided into 2 groups according to whether the serum levels of LH and FSH were always undetectable (Group A) or were detectable at some time during the 11 months (Group B). Compared with controls, testicular weight was reduced by 84% (Group A) and 78% (Group B), but the number of Leydig cells per unit area of testis was increased by a factor of 7. Despite the latter change, the binding of ¹²⁵I-hCG per 20 mg testicular homogenate was 40% lower in immunized than in control rats. The serum level of testosterone in immunized rats was ≤ 0.1 ng/ml whilst levels ranged from 0.7 to 2.9 ng/ml in controls. In the same rats the testicular production of testosterone in vitro , both basally and after incubation with hCG or dibutryl cyclic AMP, was reduced by over 90% in immunized animals, although this impairment was more severe in Group A than in Group B animals.
Leydig cell function was also assessed at 48 h after a single injection of 100 IU hCG. This treatment reduced the testicular binding of ¹²⁵I-hCG by over 89% in controls as well as both groups of immunized rats and caused a 3- to 4-fold increase in the serum levels of testosterone in all animals. Following injection of hCG, the basal production of testosterone by the testis in vitro was doubled in controls whereas this increase was over 50-fold in Group A immunized rats. In the latter, the maximum steroidogenic response of the testis in vitro was more than trebled by prior injection of hCG whilst this treatment caused a 30% reduction in the maximum response of testes from controls.     

Comparison of compensatory pituitary and testicular responses to hemicastration between prepubertal and mature rats

Prepubertal (14 days old) and mature (10 to 12 months old) male rats were hemicastrated and killed at selected intervals during a 12-week period to compare the effect of age on acute and chronic pituitary and testicular responses to hemicastration. Testis weight was increased (P less than 0.05) in hemicastrated (HC) prepubertal rats but not in mature rats compared with intact controls. After surgery, serum follicle-stimulating hormone (FSH) concentrations were elevated (P less than 0.05) by hour 12 and day 2 in prepubertal and mature rats, respectively, and remained elevated over control levels for 4 and 8 weeks, respectively. However, the magnitude of the rise in serum FSH following hemicastration was greater in the prepubertal animals. Pituitary FSH concentrations were increased (P less than 0.05) by day 1 in prepubertal HC rats and remained elevated through week 4. In contrast, pituitary FSH levels were unaffected (P greater than 0.05) by hemicastration in mature rats. Serum concentrations of inhibin-alpha were inversely related to serum FSH concentrations in prepubertal HC rats only. Serum testosterone concentrations were reduced (P less than 0.05) following hemicastration in both age groups but recovered to control levels within 24 hours. Neither serum nor pituitary concentrations of luteinizing hormone (LH) were altered by hemicastration (P greater than 0.05) in either age group. In addition, there were no changes (P greater than 0.05) in the concentrations of testicular LH or FSH receptors following hemicastration throughout the 12-week period. However, both receptor contents were increased (P less than 0.05) in prepubertal HC rats in association with the increase in testis size.(ABSTRACT TRUNCATED AT 250 WORDS)     

睾丸间质干细胞分化和移植

睾丸间质细胞是男性体内合成雄激素的主要细胞,胚胎发育期中肾胚的间质细胞及生精小管周成纤维样细胞可能是睾丸间质细胞的干细胞。在胚胎期间质干细胞分化为胎儿型间质细胞;出生后间质干细胞经间质祖细胞、未成熟间质细胞分化为成熟间质细胞。老年期间质细胞数量可能不变,但雄激素合成下降。间充质干细胞及脂肪干细胞等干细胞经诱导可分化为分泌雄激素的睾丸间质细胞,因此,间质干细胞移植可望成为治疗男性性腺功能不全和中老年雄激素缺乏的创新方法,本文对睾丸间质干细胞的分化及移植方面研究进行综述。     

Mechanisms of disease: late-onset hypogonadism

Late-onset hypogonadism (formerly called the andropause) is a clinical and biochemical syndrome associated with advancing age, which is characterized by typical signs and symptoms and a deficiency in serum testosterone levels. Age-related hypoandrogenism in the male is a result of the interaction of hypothalamopituitary and testicular factors. The hypothalamic pulsatile secretion of gonadotropin-releasing hormone is blunted, due to increased hypothalamic sensitivity to inhibition by steroids, but the responsiveness of the pituitary gonadotrophs seems to be intact. In addition, testicular volume as well as Leydig cell mass and reserve function are diminished. Taken together, these mechanisms result in reduced testosterone secretion and the loss of nycthemeral variability.     

Effect of neonatal treatment of rats with potent or weak (environmental) oestrogens,or with a GnRH antagonist,on Leydig cell development and function through puberty into adulthood

This study addressed whether reduced Sertoli cell number or manipulation of the neonatal hormone environment has an influence on final Leydig cell number per testis in the rat, by applying neonatal treatments known to affect these parameters, namely administration of a GnRH antagonist (GnRHa) or diethylstilboestrol (DES, in doses of 10, 1 or 0.1 microg per injection). The effect of treatment with either of two 'environmental oestrogens', bisphenol-A (Bis-A) or octylphenol (OP), was also evaluated. Leydig (3beta-hydroxysteroid dehydrogenase immunopositive) cell development and function (plasma testosterone levels) were studied through puberty into adulthood. Treatment with GnRHa impaired testis growth, Leydig cell (nuclear) volume per testis and testosterone levels during puberty, when compared with controls, but final Leydig cell volume/number in adulthood was comparable with controls. As adult testis weight was reduced by 45% in GnRHa-treated rats, the percentage Leydig cell volume per testis was approximately double (p < 0.01) that in controls, and also at day 35. Testosterone levels in adulthood in GnRHa-treated rats were lower (p < 0.01) than in controls but were within the lower end of the normal range. Treatment with DES caused largely dose-dependent suppression of testis growth, Leydig cell (nuclear) volume per testis and testosterone levels up to day 35. Although by adulthood, Leydig cell volume/number per testis was comparable with controls in DES-treated rats, testosterone levels remained grossly subnormal. Neonatal treatment with either Bis-A or OP had little consistent effect on any of the parameters studied except that both treatments significantly elevated testosterone levels on day 18, as did treatment with DES-0.1 microg. The present findings are interpreted in the context of what is known about the hormonal regulation of Leydig cell development. These lead to the conclusion that final Leydig cell number per testis is not determined by the number of Sertoli cells per testis and appears not to be influenced in any major way by gonadotrophins, androgens or oestrogens in the first 2 weeks of postnatal life. This implies that adult Leydig cell number may be determined prior to birth.     

睾丸移植的发展与现状

在过去的几十年中,自体睾丸移植、同种异体睾丸移植、睾丸组织块移植、Leydig细胞移植以及精原干细胞移植等方面取得了较为显著的进展。尤其是睾丸组织块移植及睾丸细胞移植方面取得的进步更是令人振奋,有望成为临床治疗男性不育症、男子性腺功能减退一种新的方法和手段。本文将就睾丸器官、组织及细胞移植发展历史及现状作一综述。     

Abnormal prolactin secretion in prepubertal boys with hypogonadotrophic hypogonadism — possible involvement in regulation of testicular steroidogenesis

The interrelationships of prolactin (Prl), gonadotrophins and testicular steroids were studied in prepuberty in 6 boys with isolated hypogonadotrophic hypogonadism (HH) and 7 boys with incomplete testicular descent (who served as controls). The boys with HH had higher basal serum levels of Prl (P less than 0.001) and LH (P less than 0.05) than the controls, but lower Prl (P less than 0.001) and LH (P less than 0.05) responses after metoclopramide + LHRH and lower testosterone responses after hCG. The peak responses of Prl after metoclopramide + LHRH and of testosterone after hCG correlated strongly in the patients as a whole (r = 0.87, P less than 0.001). These observations indicate that, as well as in the gonadotrophins, changes occur in HH in prepuberty in the synthesis and/or release of Prl. The findings also raise the possibility that Prl may play a role in the regulation of testosterone synthesis by the prepubertal testis.     

Successful islet/abdominal testis transplantation does not require Leydig cells

Pancreatic islet allo- and xenografts are not rejected and exhibit long-term beta-cell function if transplanted into the abdominal testis of the diabetic host. Successful transplantation appears dependent on local factors unique to the abdominal testis. Because Leydig cells remain viable in abdominal testes, which also retain high levels of testosterone, the following question was addressed: do Leydig cells and/or their secretory products influence islet transplantability in the successful islet/abdominal testis transplantation model? Streptozotocin-induced diabetic rats (Sprague-Dawley) were injected with 75 mg/kg ethane dimethanesulfonate (EDS) to selectively eliminate Leydig cells prior to or following transplantation with islets isolated from the BBWORdr rat. Subcutaneous silastic tubes packed with estradiol prevented Leydig cell repopulation in the EDS-treated recipient. Grafted diabetic animals, including the EDS-treated rats with serum testosterone at castration levels, became nornoglycemic following islet transplantation and remained so far for up to ten months. Leydig cells were not observed in testes of the EDS- or EDS/estradiol-treated rats, whereas the transplanted islets within these testes appeared structurally normal and highly vascularized. Islets resided within the testicular interstitial compartment and contained alpha-, beta and delta-cells, as identified by electron microscopy. Beta cells were most prominent, contained secretory granules and exhibited a close structural and functional relationship with adjacent intraislet capillaries. We conclude that Leydig cells and Leydig cell secretory products, including testosterone, are not necessary for protecting islets against rejection and they do not play an obligatory role in the success of the islet/abdominal testis transplantation protocol. Leydig cells and Leydig cell secretory products do not promote long-term beta-cell function and are not required for the return to and maintenance of normoglycemia in the grafted diabetic rat.     

Effects of maternal exposure to 3,3',4,4',5-pentachlorobiphenyl (PCB126) or 3,3',4,4',5,5'-hexachlorobiphenyl (PCB169) on testicular steroidogenesis and spermatogenesis in male offspring rats

On days 7-21 of gestation, Sprague-Dawley rats were orally administered 3 or 30 mug/kg/d of 3,3',4,4',5-pentachlorobiphenyl (PCB126) or 3,3',4,4',5,5'-hexachlorobiphenyl (PCB169) daily. Their male offspring were autopsied at 3, 6, and 15 weeks after birth to investigate the effects of the 2 polychlorinated biphenyls (PCBs) on spermatogenesis and steroidogenesis in their testes. PCB treatment caused a decrease in the area ratio of 3beta-hydroxysteroid dehydrogenase (HSD)-expressing cells (Leydig cells)/testis at 3 weeks after birth. When PCB126 was administered to pregnant rats, the plasma testosterone levels in their offspring were decreased at 3 weeks. The expression levels of P450scc, 3beta-HSD, and P450(17alpha) mitochondrial RNAs (mRNAs) were unchanged, although the StAR (steroidogenic acute regulatory protein) mRNA expression level was increased at 6 weeks. On the other hand, when PCB169 was administered, plasma testosterone levels were decreased at 3 and 6 weeks and were increased at 15 weeks. Plasma luteinizing hormone (LH) levels were decreased at 6 weeks, and plasma follicle-stimulating hormone (FSH) levels were increased at 15 weeks. The expression levels of 3beta-HSD and P450(17alpha) were increased, and the mRNA level of 5alpha-reductase 1 was decreased at 15 weeks. PCB169 treatment suppressed the conversion of round spermatids between stages VII and VIII. These results indicate that in utero and lactational exposure to PCB126 or PCB169 decreases plasma testosterone levels in 3-week-old rats, with no change in the expression levels of the mRNAs of enzymes, and that PCB169 inhibits testicular steroid synthesis more strongly than PCB126. PCB169 greatly altered the concentration of testosterone, indicating a stronger inhibitory effect on spermatogenesis. Low testosterone and LH levels in prenatally PCB169-exposed rats until 6 weeks after birth presumably retard the functional differentiation of testicular Leydig cells; however, the increased testosterone levels at 15 weeks suggest that Leydig cells in PCB-exposed rats are virtually mature by the 15th week.     

The effect of selective destruction and regeneration of rat Leydig cells on the intratesticular distribution of testosterone and morphology of the seminiferous epithelium

This study was designed to explore the relationship between the intratesticular distribution of testosterone and spermatogenesis by completely destroying the Leydig cells of mature male rats with injection of a single i.p. dose of ethane dimethanesulphonate. After such treatment, testosterone levels in serum, testicular interstitial fluid, seminiferous tubules, and whole testis declined significantly 6 to 24 hours after injection and fell below assay detection limits between 3 and 7 days. At 3 and 7 days, serum LH and FSH levels rose significantly and remained elevated up to 4 and 6 weeks, respectively, in comparison with vehicle-treated controls. Leydig cells disappeared from the interstitium by day 3, but between 2 and 4 weeks postinjection a new generation of fetal-like Leydig cells repopulated the testicular interstitium and, during weeks 6 to 10, were transformed into, or replaced by, Leydig cells with an adult type of morphology. Histologic examination of the seminiferous tubules showed progressive disruption of spermatogenesis between 3 and 14 days post-ethane dimethanesulphonate. The first histologic sign of spermatogenic damage was noted at day 3, with the occurrence of stage-specific degenerating pachytene primary spermatocytes at stages VII to VIII of the spermatogenic cycle. On day 7, these cells and degenerating round, or step 19, spermatids often were observed during stages VII to XI, although qualitatively normal spermatogenesis also was seen in these and all other stages of the cycle. Maximum impairment of spermatogenesis occurred 2 weeks post-ethane dimethane sulphonate, at which time the tubules commonly lacked one or more germ cell generations or, alternatively, showed accumulation of lipid inclusions, extracellular spaces, and variable numbers of degenerating germ cells. Following repopulation of the testis by Leydig cells during weeks 3 and 4, spermatogenesis recovered. By 10 weeks after treatment, qualitatively normal spermatogenesis was seen in the great majority of seminiferous tubules, although a few tubules still remained in which the germ cell complement was severely reduced, and contained only Sertoli cells and spermatogonia.(ABSTRACT TRUNCATED AT 400 WORDS)     

Increased testosterone production in vitro by Leydig cells from rats with severe autoimmune orchitis

We have previously observed (M. O. Suescun et al. , 1994, Journal of Andrology , 15 , 442–448) that rats with autoimmune orchitis (EAO) exhibit increased testosterone production in vitro by isolated testes. The aim of the present study was to determine whether the increase in testosterone production correlated with an enhanced number of Leydig cells and/or enhanced steroidogenic capacity per Leydig cell. For this purpose, EAO was induced in adult Sprague-Dawley rats by active immunization with testicular homogenate and adjuvants. At 80 days after the primary immunization, 60% of rats presented with severe testicular damage characterized by sloughing of the seminiferous epithelium, seminiferous tubule atrophy and interstitial mononuclear cell infiltration. At 160 days after the first immunization, testicular lesions were more severe. A morphometric study, by light microscopy, showed an increase in the number of Leydig cells in rats with EAO (45% increase at 80 days and 50% at 160 days). By electronmicroscopy, testicular sections of rats with EAO revealed the presence of numerous Leydig cells closely associated with macrophages. Most Leydig cells exhibited ultrastructural features of active steroid secreting cells.
The steroidogenic capacity of Percoll-purified Leydig cells from testes of rats with EAO, killed at 80 and 160 days, was evaluated. Leydig cells from rats with EAO exhibited an enhanced steroidogenic response to hCG in vitro at 80 days (38%) and an increase in basal (77%) and post-hCG testosterone production (115%) at 160 days compared to controls. However, these cells were less sensitive to hCG. In conclusion, the results indicate that the enhancement of in-vitro testosterone production observed in rats with EAO is accounted for both by the increased number of Leydig cells and by the increased testosterone production of each Leydig cell.     

The influence of human chorionic gonadotrophin (hCG) on the morphology of the prepubertal human undescended testis

The effect of hCG-treatment on the morphology of the undescended testis was studied in testicular biopsies from 36 prepubertal boys operated on at intervals of 1 day to 2 years after discontinuation of hormonal treatment. Immediately after treatment, mature Leydig cells were observed, and the Sertoli cells were increased in size; serum testosterone had increased to adult levels. All these changes were reversible as judged from the material taken one month or more after the last hCG injection. Based on the observations and the results of a previous study it is suggested that hCG treatment does not induce any premature onset of Sertoli cell or germ cell maturation either in the undescended or in the contralateral testis.     

Effects of photoperiod on the ultrastructure of Leydig cells in rat

The aim of this study was to examine effects of photoperiod on the ultrastructure of Leydig cells in rat. For this purpose, 21 male Wistar rats were used. Animals were divided into three groups: Control rats in group I were kept under 12 hrs light: 12 hrs dark conditions (12L: 12D) for 10 weeks. Animals in group II were exposed to long photoperiods (18L: 6D), while rats in group III were exposed to short photoperiods (6L:18D) for 10 weeks. At the end of the experiment, all animals were killed by decapitation and blood samples were obtained. Serum testosterone levels were determined with the use of a chemiluminescent enzyme immunoassay. The testes of all rats were removed and weighed, then processed for light and electron microscopy. For morphometric comparison, diameters of seminiferous tubules in each group were measured. In rats exposed to long photoperiods, testicular weights, diameters of seminiferous tubules and serum testosterone levels were significantly increased as compared to those in control rats, whereas exposure of rats to short photoperiods resulted in a significant decrease of testicular weights, diameters of seminiferous tubules and serum testosterone levels as compared to those in control rats and rats maintained in long photoperiods. The amount of mitochondria and cytoplasmic secretory granules were increased in the cytoplasm of Leydig cells of rats exposed to long photoperiods. Furthermore, an increase in extensiveness of rough endoplasmic reticulum in the cell cytoplasm was noticed in this group, whereas a decrease in mitochondria and cytoplasmic secretory granules of the Leydig cell cytoplasm was seen in rats exposed to short photoperiods. The results of our study indicate that testicular functions increase after exposure to long photoperiods and decrease after exposure to short photoperiods.     

Effect of sexual maturity on testicular injury subsequent to procarbazine administration in rats

The present study examined the effect of age on various aspects of Leydig cell and Sertoli cell function in Sprague-Dawley rats administered procarbazine. Procarbazine was administered intraperitoneally to Sprague-Dawley rats aged 14, 24, and 60 days in 3 weekly injections of 200 mg/kg. Animals were sacrificed 1 week after the last injection. Severe impairment of spermatogenesis was evident in all animals. Sertoli cell function, as assessed by total testicular ABP content, was not significantly different between procarbazine-treated animals and controls in any age group. On the other hand, procarbazine administration resulted in a 60% reduction in total intratesticular testosterone content in the 14-day-old rats but not in the 24- or 60-day-old animals. Serum testosterone was significantly reduced by 50% in the group of 14-day-old animals but not in the other age groups. Serum LH values were not significantly changed from control levels in any age group. Testicular content of Fe, Zn, Mn, and Cn were unaltered by procarbazine administration in any age group. Since serum LH and testicular cation content were not affected by procarbazine treatment, the significant decreases in serum and testicular testosterone in 14-day-old animals after procarbazine administration may indicate a direct age-dependent effect of procarbazine on Leydig cell function.     

Testicular blood flow and vasomotion can be maintained by testosterone in Leydig cell-depleted rats

The effect of testosterone supplementation on testicular blood flow, testicular vasomotion, the number of polymorphonuclear leucocytes (PMN's) in testicular blood vessels and prostatic blood flow were studied in rats in which the Leydig cell had been destroyed specifically by a single injection of ethane dimethylsulfonate (EDS). Other rats were supplemented with testosterone by subcutaneous injection of 25 mg testosterone propionate on days 1, 3 and 6. In some experiments, the effect of a single injection of 25 or 125 mg testosterone was studied. Testicular and prostatic blood flow and the number of PMN's in testicular blood vessels decreased, and vasomotion disappeared in Leydig cell-depleted rats, but testosterone supplementation restored all parameters to normal values. Moreover, a single injection of testosterone was able to restore testicular and prostatic blood flow to normal levels but had an inconsistent effect on vasomotion. These results suggest that testosterone may play a role in the physiological control of the testicular microcirculation.     

Morphological and Endocrinological Differences between the Abdominal Testes in Bilateral and Unilateral Cryptorchid Rats

Using a new experimental model of cryptorchism in rats, where testicular descent was prevented, testicular development and function were studied in bilateral and unilateral cryptorchid animals Morphometric and radioimmunological techniques were used. Up to 30 days after birth testicular development was identical in the two types of abdominal testes but in adult rats differences were observed. In these rats spermatogenesis was damaged to a similar extent, but total tubular length and testicular weight were increased in the bilateral abdominal testes. Moreover, in these testes, the volume density of Leydig cells, the total Leydig cell mass, the average Leydig cell size and the testis testosterone concentration were larger than in unilateral abdominal testes. It is suggested that the impaired spermatogenesis seen in both kinds of abdominal testes may be unrelated to Leydig cell function.