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Reversible effect of testosterone undecanoate injection on spermatogenesis in rats.

AIM: To study the effect of testosterone undecanoate (TU) injection on spermatogenesis in rats. METHODS: Twenty adult SD rats received vehicle or TU (8 mg/kg, 19 mg/kg or 625 mg/kg) injection, im, every 15 days for 60 days, and another 38 animals received similar treatments for 130 days with half of them undergoing a recovery phase of 120 days (5 rats for each treatment). At the end of the treatment, testes were removed and the diameter of the seminiferous tubules and the number of late elongated spermatids (steps 15-19) per testis were estimated with stereological methods as a measure of the spermatogenic efficiency. RESULTS: Low dose (8 mg/kg) TU treatment virtually had no effect on spermatogenesis. A dose of 19 mg/kg slightly suppressed spermatogenesis 60 days after treatment, and severe suppression occurred after another 70 days of dosing. Spermatogenesis was completely recovered at the end of the recovery phase. Large dose (625 mg/kg) TU treatment did not significantly affect spermatogenesis and was well tolerated by animals. CONCLUSION: TU injection reversibly suppresses spermatogenesis in rats.

Animals↗

Spermatogenesis and testicular tumours in ageing dogs.

The aims of this investigation were to quantify the changes in canine spermatogenesis that occur during ageing and to study the prevalence of testicular tumours and their effects on spermatogenesis in dogs. Testes from 74 dogs of various breeds without clinically detected testicular disease and from 28 dogs with clinically palpable tumours were examined. Testicular tumours were classified histologically according to the criteria of Nielsen and Kennedy (1990). Spermatogenesis was evaluated using a modified Johnsen score adapted for use in dogs. The diameter of the seminiferous tubules was measured in dogs without testicular disease to examine the possible effects of ageing. The different lifespans of small and large breeds were compensated for by expression as a percentage of the age at which dogs with various body weights are considered to be geriatric. Of the dogs without clinically detected disease, 21 of 74 had small testicular tumours. As in the 28 dogs with clinically detected tumours, multiple types of tumour and bilateral occurrence of tumours were common findings. The prevalence of tumours increased during ageing. Eighty-six per cent of the clinically detected tumours and 57% of the non-clinically detected tumours were found in geriatric dogs. The diameter of the seminiferous tubules did not change with age. Impairment of spermatogenesis was found only in dogs with bilateral tumours and in the affected testis of dogs with clinically detected tumours. In conclusion, it appears that spermatogenesis per se does not decrease during ageing in dogs. However, the occurrence of testicular tumours increases with age and this may affect spermatogenesis significantly.

Aging↗

Demonstration of direct effect of estrogen on rat spermatogenesis.

The presence of an estrogen receptor in Leydig cell cytosol suggests that estrogen could have a direct action on Leydig cell function. We have shown earlier the direct effect of estradiol on testosterone biosynthesis. We report in this communication effect of estradiol on spermatogenesis using hypophysectomized rats treated daily for four days with 400 IU hCG/Pregnyl) and 1 IU FSH (Pergonal), a model that eliminates the possibility of feedback effects of estradiol on gonadotropin secretion. Estradiol was administered in subcutaneous silastic capsules. The control animals had empty capsules. The inhibition of spermatogenesis, after estradiol treatment, was marked by the presence of multinucleated giant cells, disorganization of the germinal elements, accumulation of cellular debris and the absence of late spermatid and spermatozoa. These changes in the histoarchitecture of testis were accompanied by the reduction in the diameter of the seminiferous tubules and the thickness of the basement membrane. Morphologically Leydig cells were, however, normal. Inhibition of spermatogenesis was in relation to the amount of estrogen available/administered as estradiol capsule of 0.25 cm did not evoke significant changes in the histology of the testis whereas estradiol capsule of 4 cm caused maximum damage to the spermatogenesis. Similarly progressive damage to the spermatogenesis was quite apparent as the number of days increased after estradiol capsule implantation. Neither high (1600 IU/day/4 days) nor low /5.25 IU/day) doses of hCG synergized the effect of estradiol on spermatogenesis. Testis weight was significantly reduced after estradiol treatment but weight of the epididymis and accessory sex organs did not change. Body weight was also not effected by estradiol treatment.

Animals↗

Hypoprolactinemia does not prevent restoration of normal spermatogenesis in gonadotropin-suppressed, testosterone-replaced rats.

We have previously shown that suppression of gonadotropins and spermatogenesis can be produced in rats by immunization against gonadotropin releasing hormone (GnRH). Administration of testosterone (T) alone is effective in restoring complete spermatogenesis in these rats, although it is not effective in doing so in chronically treated hypophysectomized rats. This suggests that a pituitary factor(s) other than luteinizing hormone (LH) and follicle-stimulating hormone (FSH) is required to restore normal spermatogenesis. The studies described herein test the hypothesis that prolactin (PRL) is the additional requirement for complete restoration of spermatogenesis. Twenty rats were immunized against GnRH, and four groups of five each received either 1) 24-cm T-filled Silastic implant (TSl), 2) TSl plus bromocriptine pellet (B), 3) B plus empty Silastic implant (Sl), or 4) Sl alone. Five nonimmunized rats received Sl alone and served as controls. All rats were sacrificed 2 months after treatment. GnRH immunization and B administration suppressed gonadotropins and PRL levels, respectively, and advanced spermatids were not detectable in these rats. Testis weight was suppressed to about 19% of controls. The number of advanced spermatids in control rats was 220 +/- 23 x 10(6). TSl administration restored advanced spermatids to numbers comparable to controls in GnRH-immunized rats whether the rat received B (191 +/- 17 x 106) or not (217 +/- 18 x 10(6)). Additionally, we determined mRNA levels for PRL and FSH beta subunit (FSH beta) in the pituitary by Northern blot and densitometric scanning. The mRNA levels of PRL mirrored serum PRL levels, and the same was true for FSH beta subunits and serum FSH levels. These data show that suppression of PRL has no effect on the ability of T to restore complete spermatogenesis in GnRH-immunized rats. This observation mitigates against the hypothesis that PRL is the pituitary factor required to allow complete restoration of spermatogenesis to occur.

Age Factors↗

Neonatal exposure of male rats to estradiol benzoate causes rete testis dilation and backflow impairment of spermatogenesis.

Estrogens administered to perinatal rodents cause spermatogenesis impairment; this study was undertaken to determine the mechanisms by which estrogens exert this effect. Neonatal male Wistar rats received estradiol benzoate (either 0.5 mg/5g BW or 1 mg/5g BW) and were killed at days 10, 22, 33, 45, and 60. Controls received vehicle. In tubule cross-sections of transverse sections of the right testes, 1) tubular diameter (TD) and seminiferous epithelium height (SEH) were measured, 2) normal and impaired spermatogenesis were classified in terms of the most advanced germ cell type present, including tubules lined by Sertoli cells only. A significant dose-dependent rise in the tubule percentage lined by Sertoli cells only at day 60 reflected spermatogenesis impairment. This was evidenced by the presence of multinucleated germ cells in a thin epithelium and sloughed into an enlarged tubular lumen, which was reflected in a significant dose-dependent increase in TD/SEH values from day 22 onward. TD was significantly greater and SEH significantly lower in tubular segments located at the cranial than the caudal halves of rat testes treated with the high (days 22, 33, and 60) and the low dose (day 33). This indicated distension in cranial tubular segments, perhaps due to the fact that these segments were the closest to the dilated rete testis. Consequently, they showed the highest TD/SEH values and the most regressive features of spermatogenesis (tubules lined by Sertoli cells only). In contrast, caudal segments in rat testes treated with the low dose showing TD/SEH values similar to controls displayed a delayed maturation of spermatogenesis coinciding with the late appearance of mature Leydig cells.

Age Factors↗

Essential requirement for both hsf1 and hsf2 transcriptional activity in spermatogenesis and male fertility.

Heat shock factors (Hsfs) are major transactivators of heat shock proteins but are also involved in regulation of other genes active in embryonic development. High expression levels of Hsfs in mouse testis during development suggest a role for these factors in spermatogenesis, a cyclic process of spermatogonia cell-differentiation into mature spermatozoa. In contrast to hsf1(-/-) mice, which exhibit normal spermatogenesis, targeted disruption of hsf2 results in reduced testicular size but only a small impairment in male fertility. We show here that disruption of both hsf1 and hsf2 results in a more severe phenotype associated with male sterility due to severe defects in spermatogenesis. Earliest defects observed are the reduced number of germ cells in juvenile mice and germ cells that enter the meiotic prophase fail to progress beyond the pachytene stage. This was associated with a reduction or absence of transcription of genes critically involved in spermatogenesis. The findings suggest that additive or synergistic transcriptional activity of both hsf1 and hsf2 is required for normal mammalian spermatogenesis and male fertility.

Animals↗

Spermatogenesis in nonmammalian vertebrates.

Spermatogenesis appears to be a fairly conserved process throughout the vertebrate series. Thus, spermatogonia develop into spermatocytes that undergo meiosis to produce spermatids which enter spermiogenesis where they undergo a morphological transformation into spermatozoa. There is, however, variation amongst the vertebrates in how germ cell development and maturation is accomplished. This difference can be broadly divided into two distinct patterns, one present in anamniotes (fish, amphibia) and the other in amniotes (reptiles, birds, mammals). For anamniotes, spermatogenesis occurs in spermatocysts (cysts) which for most species develop within seminiferous lobules. Cysts are produced when a Sertoli cell becomes associated with a primary spermatogonium. Mitotic divisions of the primary spermatogonium produce a cohort of secondary spermatogonia that are enclosed by the Sertoli cell which forms the wall of the cyst. With spermatogenic progression a clone of isogeneic spermatozoa is produced which are released, by rupture of the cyst, into the lumen of the seminiferous lobule. Following spermiation, the Sertoli cell degenerates. For anamniotes, therefore, there is no permanent germinal epithelium since spermatocysts have to be replaced during successive breeding seasons. By contrast, spermatogenesis in amniotes does not occur in cysts but in seminiferous tubules that possess a permanent population of Sertoli cells and spermatogonia which act as a germ cell reservoir for succeeding bouts of spermatogenic activity. There is, in general, a greater variation in the organization of the testis and pattern of spermatogenesis in the anamniotes compared to amniotes. This is primarily due to the fact there is more reproductive diversity in anamniotes ranging from a relatively unspecialized condition where gametes are simply released into the aqueous environment to highly specialized strategies involving internal fertilization. These differences are obviously reflected in the mode of spermatogenesis and this is particularly true of the stage of spermiogenesis where the morphology of the species-specific spermatozoon is determined. Moreover, unlike amniotes, many anamniotes display a spermatogenic wave manifest, depending upon the species, either at the level of the cyst or seminiferous lobule. This variation in the organization of the testis makes certain anamniotes perfect models for investigating germ cell development and maturation. For instance, the presence of a spermatogenic wave provides an opportunity to manually isolate discrete germ cell stages for analysis of specific Sertoli/germ cell interactions. Furthermore, for many anamniotes, germ cells mature in association with a morphologically poorly developed Sertoli cell. This seeming independence of Sertoli cell regulation allows the in vitro culture of isolated germ cells of some species of anamniotes through several developmental stages. Thus, due either to the anatomical organization of the testis, or structural simplicity of the germinal units, nonmammalian vertebrates can provide excellent experimental animal models for investigating many basic problems of male reproduction.

Animals↗

Stage-specific and tissue-specific expression characteristics of differentially expressed genes during mouse spermatogenesis.

Spermatogenesis occurs in successive mitotic, meiotic, and post-meiotic phase, and involves a number of unique processes including meiosis and dramatic morphological changes. The unique differentiation mechanisms of spermatogenesis suggest the existence of germ-cell-specific molecules. The most straight forward strategy to elucidate differentiation mechanisms is to identify and characterize differentiation-specific molecules and their associated genes in germ cells. However, only a few genes specifically involved in spermatogenesis have been studied. In the present study, six different types of spermatogenic cells (primitive type A spermatogonia, type B spermatogonia, preleptotene spermatocytes, pachytene spermatocytes, round spermatids, and elongating spermatids) were isolated from Balb/c mice testes using velocity sedimentation and Atlas cDNA arrays containing 1,176 known mouse genes were used to determine the gene expression profiles of the spermatogenic cells. The expression of 260 genes were detected in six different stages of spermatogenic cells and a number of genes showed differential expression. The 23 differentially expressed genes were further analysed by reverse transcription polymerase chain reaction (RT-PCR) for their stage-specific and tissue-specific expression characteristics. Based on the results of RT-PCR, six genes highly express in both primitive type A and type B spermatogonia, four genes up-regulate in type B spermatogonia, two genes up-regulate in spermatocytes, two genes up-regulate in spermatids, three genes express constantly from primitive A spermatogonia to elongating spermatids, two genes express constantly from primitive A spermatogonia to round spermatids, two genes do not change in their expression during spermatogenesis, two genes can be detected highly in adult testis, but are undetectable in spermatogenic cells. The tissue-specific expression characteristics of the 23 genes showed that some of them specifically expressed in testes or other tissues. These data provide new information for further studies into spermatogenesis-related genes and may lead to the identification of genes with potential relevance to the differentiation of spermatogenic cells. In addition, some of these genes could be considered to be used as the molecular markers for different stages of spermatogenic cells.

Animals↗

Developmentally regulated expression of Hsp70-2 and a Hsp70-2/lacZ transgene during spermatogenesis.

Germ cells synthesize large amounts of HSP70-2 protein during the meiotic phase of spermatogenesis. This developmentally regulated expression of HSP70-2 contrasts with the constitutive or inducible expression of other 70-kDa heat shock proteins (HSP70s). To better understand the genetic regulation of Hsp70-2, we used mRNA primer- extension, reverse transcriptase PCR (RT-PCR), and cDNA sequencing to determine that transcription began as far as 353 bp upstream of the start codon. We also identified a previously unrecognized 239-bp intron which is spliced out of the pre-mRNA transcript to leave a 114 nt 5'-untranslated region. Transgenic mice were then produced to delimit the upstream regulatory region required for developmental expression of Hsp70-2 during spermatogenesis. Results with multiple lines of transgenic mice containing promoter-reporter transgenes with varying lengths of Hsp7-2 sequence indicate that promoter sequences up to 640 bp upstream of the start codon and 287 bp upstream of the transcription start site are required for Hsp70-2/lacZ expression in spermatocytes. Histochemical detection of transgene beta- galactosidase activity was coincident with immunohistochemical detection of HSP70-2 protein, both in the first wave of spermatogenesis in juvenile mice and in ongoing spermatogenesis of adult mice. The distribution of Hsp7O-2 and Hsp7O-2/lacZ mRNAs was determined by Northern blot, in situ hybridization, and RT-PCR, and it was found that upregulation of expression of both Hsp7O-2 and Hsp7O-2/lacZ was specific to the meiotic phase of spermatogenesis.

Animals↗

Spermatogenesis: its regulation by testosterone and FSH.

It has been clear for decades that testosterone is a necessary prerequisite for the maintenance of established spermatogenesis in the adult testes, and for the restoration of spermatogenesis in testes induced experimentally to become azoospermic. In contrast, the possible involvement of FSH in regulating spermatogenesis in the adult mammal, though also studied extensively, continues to be debated in the literature. The mechanisms by which testosterone and FSH regulate spermatogenesis remain uncertain as well. This review focuses on our current understanding of the involvement of testosterone and of FSH in the maintenance and restoration of spermatogenesis in the adult testes, and discusses the emerging concept that testosterone and FSH serve as cell survival factors.

Animals↗

Testosterone and FSH have independent, synergistic and stage-dependent effects upon spermatogenesis in the rat testis.

Adult rats were hypophysectomized and treated with ethane dimethanesulphonate (EDS) selectively to eliminate the Leydig cells in the testis. By removing the source of endogenous gonadotrophins and androgens, the subsequent effects on the seminiferous epithelium were studied after 20 days of treatment with vehicle, or FSH (2 x 50 micrograms/day) or a low dose of testosterone (0.6 mg testosterone esters every 3rd day) alone or in combination. Compared to vehicle-treated hypophysectomized rats with Leydig cells, testis weight in saline-treated hypophysectomized rats treated with EDS declined by 50%, spermatogenesis was disrupted severely and only 18% of the tubules contained spermatids, these being confined to stages I-VI of the spermatogenic cycle. Treatment with either FSH or testosterone esters alone significantly (P less than 0.01) increased testis weight compared to vehicle-treated hypophysectomized rats treated with EDS and 40% of tubules contained spermatids either at stages I-VI after FSH, or at all stages I-XIV after testosterone treatment. Treatment with FSH and testosterone esters together maintained testis weights approximately 20% above vehicle-treated hypophysectomized controls; over 70% of the seminiferous tubules contained spermatids and there was a marked stimulation of spermatogenesis at all stages of the spermatogenic cycle. The results suggest, that in the absence of the pituitary gland and the Leydig cells, FSH alone partially supports spermatogenesis up to the development of round spermatids whereas testosterone is capable of maintaining spermatid development at all 14 stages of the cycle. When FSH and testosterone were administered in combination, the effects upon spermatogenesis were far greater than the response expected if their individual effects were simply additive. It is therefore concluded that FSH may play a role in normal spermatogenesis and that this role is essentially that of augmenting the response of the testis to testosterone. The biochemical mechanisms via which this might occur are discussed and hypophysectomized rats treated with EDS used in the present studies should provide a useful approach for their identification.

Animals↗

Quantitative estimation of spermatogenesis in bulls (Bos indicus) in a tropical environment of Nigeria.

Spermatogenesis in bulls (Bos indicus) indigenous to Nigeria, and the significance of Sertoli cell index (SCI) as a measure of testicular degeneration were studied. The mean testicular weights and dimensions were lower than reported for Bos taurus breeds. The diameters of the seminiferous tubules were lower than reported for Bos taurus, although within the same range. Inter-month and intra-month variations were highly significant (P less than 0.01). A mean annual spermatogenesis of 77.60% was reported. Active spermatogenesis was observed throughout the year, with a peak during the rainy season and extending toward the pre-dry season. This was consistent with previous reports. Severe testicular degeneration was found to influence spermatogenesis. This was reflected in the decrease in SCI. Mild degeneration had no significant effect on spermatogenesis, and did not significantly change the SCI. The SCI was defined as the ratio of the number of germinal cells to the number of Sertoli cells in the same cross sections of tubules.

Animals↗

A spermatogenesis-related gene expression profile in human spermatozoa and its potential clinical applications.

Spermatogenesis is an essential stage in the human reproductive process. In a previously study aiming to determine which genes might be involved in spermatogenesis, we compared the gene expression profiles of adult and fetal testes by hybridizing cDNA probes prepared from adult and fetal testes to membranes dotted with gene clones derived from a commercial human testis library. We identified 266 differentially expressed genes that showed higher expression levels in adult testes, indicating their potential roles in spermatogenesis. In the present study, we applied the same cDNA microarray technique to the analysis of gene expression in the spermatozoa of normal fertile men and found 149 genes that were expressed at higher levels in adult testis. A further study of five sperm motility-related genes selected from this profile by real-time PCR revealed that there was significant difference in the expression levels of two genes ( TPX-1, testis-specific protein 1 and LDHC, lactate dehydrogenase C, transcript variant 1) between normal ( n=29) and motility impaired ( n=24) semen samples, indicating that these genes are involved in sperm function. Our results demonstrated that spermatogenesis-related gene profiling could help to assess sperm quality in humans, and further study of these genes will help us to elucidate the mechanisms involved in spermatogenesis and diseases relating to human infertility.

A Kinase Anchor Proteins↗

Endocrine control of human spermatogenesis.

We performed a series of studies in normal men to determine the relative roles of FSH and LH in the regulation of human spermatogenesis. Experimental gonadotropin deficiency was induced in normal men by administration of high-dosage testosterone (T) enanthate, resulting in suppression of spermatogenesis to severely oligospermic or azoospermic levels. In these gonadotropin deficient normal men, we found that selective replacement of either LH activity, with human chorionic gonadotropin (hCG) or hLH, or FSH activity with hFSH increased sperm counts into the 20-50 million/ml range, but quantitatively normal spermatogenesis was not achieved. To determine whether both LH and FSH together are required for quantitatively normal spermatogenesis, selective FSH deficiency was induced in normal men by administration of hCG. In the setting of high LH-like activity and markedly suppressed FSH levels induced by hCG, sperm production was partially suppressed again into the 20-50 million/ml range. Replacement of FSH activity, with either hFSH or human menopausal gonadotropin in hCG-treated normal men stimulated sperm production into the control range in all subjects. These studies demonstrate that neither normal serum levels of FSH or LH are required for qualitatively normal spermatogenesis in man, since sperm counts in the range of 20-50 million/ml are found in states of selective FSH or LH deficiency. However, normal levels of both FSH and LH are required to achieve quantitatively normal sperm production in man.

Chorionic Gonadotropin↗

Persistence of spermatogenesis in hypogonadotropic hypogonadism treated with testosterone.

The case histories are reported of two patients who had persistent spermatogenesis as evidenced by normal semen analyses and fertility in the face of hypogonadotropic hypogonadism and testosterone administration. When not receiving testosterone, both men consistently had normal or low serum gonadotropin levels. Since pooled serum testosterone levels were low simultaneously, these "normal" gonadotropin values are still consistent with hypogonadotropic hypogonadism. Standard testosterone replacement therapy maintained secondary sex characteristics and, surprisingly, spermatogenesis in both men. A review of the literature revealed conflicting evidence concerning the roles of gonadotropins and testosterone in affecting spermatogenesis. In applying this evidence to our patients, it appears that gonadotropins may have only a minimal role in maintaining fertility in patients with established spermatogenesis and "adequate" testosterone levels; it also appears that relatively low doses of exogenous testosterone may maintain or enhance spermatogenesis in certain individuals. We conclude that men with acquired hypogonadotropic hypogonadism should not be presumed to be sterile and that a larger study of fertility in these patients is necessary. Until then, we recommend that the semen of these patients be analyzed at the time of diagnosis and during treatment with testosterone.

Adult↗

The effect of testicular nongerm cell tumors on local spermatogenesis.

OBJECTIVE: To assess ipsilateral spermatogenesis in men with malignant and benign nongerm cell tumors of the testis. DESIGN, PATIENTS: Histologic review of radical orchiectomy specimens performed for 20 men with malignant nongerm cell tumors and 15 with benign testicular lesions, including five Leydig cell tumors with benign clinical features. MAIN OUTCOME MEASURES: Degree of spermatogenesis was determined on a 1 to 10 scale, with 10 representing mature sperm within a seminiferous tubule. For each patient "near" and "far" scores were determined by obtaining the mean score of 50 tubules adjacent (< 3 mm) to the tumor and 50 tubules distant (> 3 mm) from the tumor, respectively. RESULTS: Total, near, and far scores were all lower for malignant tumors than for benign lesions. Scores for Leydig cell tumors were similar to benign lesions. Malignant tumors demonstrated a gradient effect, with greatest impairment of spermatogenesis occurring adjacent to tumor. In contrast, a distinction between near and far scores was not observed for benign lesions or Leydig cell tumors. CONCLUSIONS: Malignant nongerm cell tumors of the testis were associated with significant impairment of ipsilateral spermatogenesis, particularly in areas adjacent to tumor. These findings are similar to those observed for testicular germ cell tumors, suggesting a generalized negative influence on ipsilateral spermatogenesis by malignant tumors.

Adult↗

Microdeletion of the DAZ (deleted in azoospermia) gene or the YRRM (Y chromosome ribonucleic acid recognition motif) gene does not occur in patients with Klinefelter's syndrome with and without spermatogenesis.

OBJECTIVE: To evaluate the occurrence of microdeletions of the Y chromosome involving the DAZ and YRRM genes in patients with Klinefelter's syndrome with and without spermatogenesis. DESIGN: Controlled clinical study. SETTING: Yamagata University Hospital, Yamagata, Japan. PATIENT(S): Patients with Klinefelter's syndrome with spermatogenesis (n = 1) and without spermatogenesis (n = 20) and a control group of men of proven fertility (n = 10). INTERVENTION(S): Blood and semen sampling and testicular biopsy. MAIN OUTCOME MEASURE(S): Semen analysis, polymerase chain reaction amplification of 32 DNA loci on the long arm of the Y chromosome involving the DAZ (deleted in azoospermia) and YRRM (Y chromosome ribonucleic acid recognition motif) genes, and measurement of plasma FSH, LH, and testosterone levels. RESULT(S): No microdeletions of 32 loci were found in any of the patients with Klinefelter's syndrome, either with or without spermatogenesis. Plasma LH and FSH levels were abnormally high and testosterone levels were reduced in all the patients with Klinefelter's syndrome. American Society for Reproductive Medicine.) CONCLUSION(S): Severe impairment of spermatogenesis in patients with Klinefelter's syndrome is not caused by microdeletions of the Y chromosome involving the DAZ and YRRM genes.

DNA↗

Canine model of infertility after spinal cord injury: time course of acute changes in semen quality and spermatogenesis.

PURPOSE: We established a canine model of subfertility after spinal cord injury and examined the time course of acute changes in semen quality and spermatogenesis after spinal cord injury. MATERIALS AND METHODS: Seven dogs underwent surgical T7 spinal cord injury. Six dogs were used as controls. Electroejaculation and testicular fine needle aspiration were performed at baseline and twice weekly for 3 weeks after spinal cord injury. Semen quality change was examined by standard semen analysis. Spermatogenesis was assessed by flow cytometry of testicular fine needle aspiration in all dogs as well as by testicular histology at study conclusion in 4 controls and 4 spinal cord injured dogs. RESULTS: No significant changes in spinal cord injured dogs were noted before 3 weeks after injury. From baseline to 3 weeks after injury certain changes were evident in spinal cord injured dogs. Mean antegrade sperm motility decreased from 62.9% to 20.1% (p = 0.008), mean total sperm (antegrade plus retrograde total sperm) decreased from 423 to 294 x 106 which was not statistically significant, and the incidence of testicular haploid cells decreased from 75.6% to 48.3% (p = 0.028). No significant change in any parameter was present in control dogs. The mean number of mature spermatids per cross-sectional tubule on final testicular histology was significantly decreased in spinal cord injured dogs compared with controls (13.6 versus 43.9, p = 0.02). CONCLUSIONS: In the canine model tested the dogs readily survived spinal cord injury, electroejaculation was effective for obtaining ejaculate and fine needle aspiration allowed serial examination of spermatogenesis. Three weeks after spinal cord injury but not before 3 weeks sperm motility and spermatogenesis were significantly decreased. However, at the same point this decrease in spermatogenesis was not yet reflected in the total ejaculated sperm count.

Animals↗