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PubMed2006

Correlation of the size of undescended testis with its locations in vatrious age groups.

OBJECTIVE: To assess the correlation of the size of undescended testis with its location in children of various age groups, per-operatively. DESIGN: Cross-sectional study. PLACE AND DURATION OF STUDY: Surgical Unit B, National Institute of Child Health, Karachi from February 2004 - November 2005. PATIENTS AND METHODS: Children presenting with undescended testis at surgical outpatient were recruited. Physical examination and relevant investigations (haemoglobin, ultrasound for location and size of testes) were performed. Patients were divided randomly into three age groups, group I (8 months - 2.5 years), group II (2.6 - 8 years), group III (8.1-13 years). At orchiopexy location and size of undescended testis were noted. Patients were further sub-divided into groups according to peroperative location of undescended testis, group A (intra-abdominal), group B (intra-canalicular), group C (distal to superficial inguinal ring - pubic). Where no testis was found, a separate group D was assigned. The size of undescended testis at different locations in various age groups was compared with reference to normal descended testicular size in the respective age group, for statistical significance. ANOVA test was used for intergroup comparison for the size of undescended testis and Student t- test was applied for comparison with reference to normal values of the size of testis. RESULTS: A total of 102 patients with undescended testis were included in the study. The total number of 107 testicular units were assessed. Group I had 28, group II, 41 and group III, 38 testes. There were 24 intra-abdominal, 68 intra-canalicular and 12 pubic in location. In 3 cases, no testis was found at exploration. We found no statistically significant difference amongst groups (p-value=0.090) between the size of the undescended testis at different peroperative locations. The size of undescended testis grew with the age as undescended testis of larger size were found in older age group as compared to younger age group. By applying Student t-test, we did not find statistically significant difference in relation to the size of undescended testis in various age groups in comparison to the reference of mean volume of normally descended testis in the respective age groups. CONCLUSION: Pre-pubertal size of undescended testis does not differ significantly from that of normal reference value of descended testis in relation to age and location. The ultimate size of the testis can only be assessed after puberty whether it is a normally descended or undescended testis.

Adolescent↗
PubMed2003

Measurement of the linear dynamics of the descent of the bovine fetal testis.

Measurements were made on 86 male bovine fetuses collected from abattoirs in the vicinity of Sydney, Australia. The fetal body length was used to calculate the approximate day of gestational age (DGA); most fetuses were between 60 and 150 DGA. The distances from the caudal pole of the kidney (metanephros) to, respectively, the tip of the scrotum, the distal end of the testis and the internal ring of the inguinal canal were measured, as well as the dimensions of the testis and gubernaculum testis. Distances of (1) testis to inguinal canal, (2) inguinal canal to scrotum, (3) testis to scrotum and (4) gubernaculum to scrotum were calculated from these measurements, which were made on both left and right sides. The total length of the gubernaculum testis increased during transabdominal passage and during transinguinal passage of the testis. Furthermore, the gubernaculum appeared to maintain the testis at a relatively fixed distance from the scrotum during transabdominal passage so that the inguinal canal appeared to move towards the testis. The greatest distance between the testis and the tip of the scrotum was found during the transinguinal passage of the testis and was 2.8 cm for the left testis and 2.3 cm for the right. When located within the scrotum, each testis was still 1.6-1.7 cm from the tip of the scrotum, so the distance to be traversed was only 0.6-1.2 cm. Following passage of the testis through the inguinal canal, the gubernaculum became shorter and its distal tip was displaced toward the distal end of the scrotum. Traction by the gubernaculum could account for the final transposition of the testis from the external inguinal ring to the scrotum. Other factors involved in displacement of the testis include differential growth patterns as well as increases in the dimensions of the testis itself.

Animals↗
PubMed2000

Role of transforming growth factor-alpha and the epidermal growth factor receptor in embryonic rat testis development.

Embryonic testis development requires the morphogenesis of cords and growth of all cell populations to allow organ formation. It is anticipated that coordination of the growth and differentiation of various cell types involves locally produced growth factors. The current study was an investigation of the hypothesis that transforming growth factor-alpha (TGF-alpha) is involved in regulating embryonic testis growth. TGF-alpha has previously been shown to function in the postnatal testis. TGF-alpha and other members of the epidermal growth factor (EGF) family act through the epidermal growth factor receptor (EGFR) to stimulate cell proliferation and tissue morphogenesis. To understand the potential actions of TGF-alpha in the embryonic testis, general cell proliferation was investigated. Characterization of cell proliferation in the rat testis throughout embryonic and postnatal development indicated that each cell type has a distinct pattern of proliferation. Germ cell growth was transiently suppressed around birth. Interstitial cell growth was high embryonically and decreased to low levels around birth. A low level of Sertoli cell proliferation was observed at the onset of testis cord formation. Sertoli cell proliferation in early embryonic development was low; the levels were high later in embryonic development and remained high until the onset of puberty. Both TGF-alpha and the EGFR were shown to be expressed in the embryonic and postnatal rat and mouse testis. Perturbation of TGF-alpha function using neutralizing antibodies to TGF-alpha on testis organ cultures dramatically inhibited the growth of both embryonic and neonatal testis. TGF-alpha antibodies had no effect on cord formation. The TGF-alpha antibody was found to be specific for TGF-alpha in Western blots when compared to EGF and heregulin. Testis growth was also inhibited by perturbation of EGFR signaling using an EGFR kinase inhibitor. Therefore, TGF-alpha appears to influence embryonic testis growth but not morphogenesis (i.e., cord formation). Treatment of embryonic testis organ cultures with exogenous TGF-alpha also perturbed development, leading to an increased proliferation of unorganized cells. Testis from EGFR and TGF-alpha knockout mice were analyzed for testis morphology. TGF-alpha knockout mice had no alterations in testis phenotype, while EGFR knockout mice had a transient decrease in the relative amount of interstitial cells before birth. Observations suggest that there may be alternate or compensatory factors that allow testis growth to occur in the apparent absence of TGF-alpha actions in the mutant mice. In summary, the results obtained suggest that TGF-alpha is an important factor in the regulation of embryonic testis growth, but other factors will also be involved in the process.

Animals↗
PubMed2006

The high scrotal ("gliding") testis revised.

BACKGROUND: At present, the high scrotal testis is considered a distinct and separate entity of undescended testis. OBJECTIVES: The aim of this study was to assess whether high scrotal testis is actually either a congenital- or acquired-undescended testis. DISCUSSION: In 527 consecutive boys (aged 0.4 to 16.5 years, mean 7.5) referred for non-scrotal testis, the number of high scrotal testis was prospectively determined. According to previous testis position, the high scrotal testis was classified into congenital- and acquired-high scrotal testis. In congenital-high scrotal testis orchidopexy was performed whereas spontaneous descent at puberty was awaited in acquired-high scrotal testis. In 210 testes, the gonad was diagnosed as high scrotal. In six testes the condition was congenital and 204 testes were diagnosed as acquired. All cases of congenital-high scrotal testis were treated surgically. In 100 acquired-high scrotal testis follow-up was performed. Of these, 75 testes descended spontaneously at puberty. CONCLUSION: We propose that the high scrotal testis should be regarded, not as a distinct and separate entity, but as a part of the spectrum of either congenital-undescended testis or acquired-undescended testis. Since spontaneous descent can occur at puberty in acquired-high scrotal testis, therapy may be different between both forms.

Adolescent↗
PubMedDate not supplied

Expression, action, and regulation of transforming growth factor alpha and epidermal growth factor receptor during embryonic and perinatal rat testis development.

The objective of the current study was to extend previous observations and examine the expression pattern and effects of transforming growth factor alpha (TGFalpha) and epidermal growth factor receptor (EGFR) on embryonic testis morphogenesis and growth. The expression of TGFalpha was determined after morphological sex determination (seminiferous cord formation at embryonic day 13 [ED13]) through perinatal testis development (postnatal day 5 [PD5]) with a quantitative reverse transcription-polymerase chain reaction procedure. Expression of messenger RNA (mRNA) for TGFalpha appeared to be more dynamic during testis development when compared with the expression of mRNA for EGFR. Message for TGFalpha was reduced at ED16 and PD4, and was elevated at PD0 during testis development. In contrast, EGFR mRNA levels were negligible at ED15 and were elevated constitutively from ED16 through PD5. Immunohistochemistry was conducted at ED14, ED16, ED19, PD0, PD3, and PD5 to localize cellular expression of both TGFalpha and EGFR. At ED16, positive staining for EGFR was localized to the cords, and by ED19, was mainly in the cords with slight expression in the interstitium. From PD0 to PD5, positive staining for EGFR was detected in the germ, Sertoli, and interstitial cells. Immunohistochemistry for TGFalpha detected localization at ED14 and ED16 to the Sertoli cells and to specific cells in the interstitium. From ED19 through PD5, TGFalpha was detected in the Sertoli, germ, and interstitial cells, and in endothelial cells within the interstitium. To determine the effects of TGFalpha on embryonic testis growth and seminiferous cord formation, ED13 testis organ cultures were treated with sense and antisense TGFalpha oligonucleotides. Antisense TGFalpha inhibited testis growth by 25%-30% in ED13 testis organ cultures when compared with sense oligonucleotide control pairs. To examine the effects of TGFalpha on perinatal testis growth, PD0 testis cultures were treated with different doses of TGFalpha. TGFalpha increased thymidine incorporation into DNA in PD0 testis cultures. Therefore, TGFalpha appears to have actions on both embryonic and perinatal testis growth. The regulation of TGFalpha and EGFR mRNA levels were examined using PD0 testis cultures treated with hormones that stimulate testis growth. Follicle-stimulating hormone (FSH) stimulated (P < .05) and testosterone tended to stimulate (P < .07) mRNA expression of EGFR. Epidermal growth factor stimulation of PD0 testis cultures did not affect levels of mRNA expression for EGFR, but did suppress expression of mRNA for TGFalpha. These results taken together demonstrate that TGFalpha can act to regulate early embryonic and perinatal testis growth. Furthermore, TGFalpha and EGFR expression can be regulated through growth stimulatory hormones such as FSH and testosterone.

Animals↗
PubMed1999

Expression and action of transforming growth factor beta (TGFbeta1, TGFbeta2, and TGFbeta3) during embryonic rat testis development.

The objective of the current study was to determine the role of transforming growth factor beta (TGFbeta) during seminiferous cord formation and embryonic testis development. The expression pattern of mRNA for TGFbeta isoforms was evaluated during testis development through a quantitative reverse transcription-polymerase chain reaction (QRT-PCR) procedure. Expression of mRNA for TGFbeta1 was highest at postnatal day 0 (P0) and P10. In contrast, TGFbeta2 was high at embryonic day 15 (E15), declined at E16, and showed a transient increase at P0 through P3 of testis development. Interestingly, expression of mRNA for TGFbeta3 was high during embryonic development and then declined after P3. Immunohistochemical localization of TGFbeta1 and TGFbeta2 demonstrated expression in Sertoli cells at E14 and in the seminiferous cords at P0. Selective interstitial cells expressed high concentrations of TGFbeta1 and TGFbeta2 in P0 testis. TGFbeta3 was expressed in selective cells at the junction of the E14 testis and mesonephros. The cells expressing TGFbeta3 in the testis appeared to be preperitubular cells that resided around the seminiferous cords. TGFbeta3 was localized to gonocytes in P0 testis. TGFbeta1 was found to have no influence on seminiferous cord formation in embryonic organ cultures of E13 testis. In contrast, growth of both E13 and E14 embryonic organ cultures was inhibited by TGFbeta1 and resulted in reduced testis size (40% of controls) with fewer cords present. A P0 testis cell culture and thymidine incorporation assay were used to directly examine the effects of recombinant TGFbeta1. TGFbeta1 alone had no influence on thymidine incorporation in P0 testis cell cultures when compared to controls. Interestingly, TGFbeta1 inhibited epidermal growth factor (EGF), and 10% calf serum stimulated P0 testis cell growth but not FSH-stimulated growth. Therefore, TGFbeta1 appears to inhibit testis growth in both the embryonic and early postnatal periods. The hormonal regulation of TGFbeta expression was measured using P0 testis cell cultures and a QRT-PCR procedure for each TGFbeta isoform. High concentrations of EGF stimulated expression of mRNA for TGFbeta1 after 24 h but suppressed expression of TGFbeta3. In contrast, there was no effect of FSH on TGFbeta isoform expression. In summary, TGFbeta regulates embryonic and P0 testis growth through inhibiting the actions of positive growth factors such as EGF. In addition, EGF but not FSH appears to regulate TGFbeta isoform expression. Combined observations from the present study demonstrate that TGFbeta isoforms are differentially expressed and appear to be regulators of testis growth during the embryonic and early postnatal periods.

Animals↗
PubMed2000

Role of neurotropins in rat embryonic testis morphogenesis (cord formation).

The process of seminiferous cord formation is the first morphological event that differentiates a testis from an ovary and indicates male sex determination. Cord formation occurs by embryonic Day 14 (Day 0 = plug date; E14) in the rat. A series of experiments were conducted to determine if neurotropins and their receptors are important for the process of rat embryonic cord formation. The expression of low affinity neurotropin receptor (p75/LNGFR) was determined by immunohistochemistry on sections of both testis and ovary from E13 through birth (Day 0, P0) with an antibody to p75/LNGFR. The staining for p75/LNGFR was present in the mesonephros of E13 gonads and in a sex-specific manner appeared around developing cords at E14 in the embryonic testis. At birth, staining for p75/LNGFR was localized to a single layer of cells (i.e., peritubular cells) that surrounded the seminiferous cords. The genes for both neurotropin 3 (NT3) and for corresponding high affinity neurotropin trkC receptor were found to be expressed in the E14 rat testis, as well as other neurotropins and receptors. Immunocytochemical analysis of E14 rat testis demonstrated that NT3 was localized to the Sertoli cells and trkC was present in individual cells of the interstitium at E16 and in selected preperitubular cells at E18. Previously, the peritubular cells adjacent to the cords were demonstrated to be derived from migrating mesonephros cells around the time of cord formation. To determine if neurotropins were involved in cord formation, the actions of neurotropins were inhibited. A high affinity neurotropin receptor (trk)-specific kinase inhibitor, K252a, was used to treat organ cultures of testes from E13 rats prior to cord formation. Treatment of E13 testis organ cultures with K252a completely inhibited cord formation. K252a-treated organ cultures of E14 testis that contained cords did not alter cord morphology. A second experiment to inhibit neurotropin actions utilized a specific antagonist trk-IgG chimeric fusion protein and E13 testis organ cultures. The trk-IgG molecules dimerize with endogenous trk receptors and inhibit receptor signaling and activation of ligand function. Forty percent of E13 testis organ cultures treated with trkC-IgG had significantly reduced cord formation. TrkA-IgG had no effect on initiation of cords; however, in fifty percent of the treated organs, a "swollen" appearance of the cord structures was observed. Experiments using trkB-IgG chimeric protein on E13 organ cultures had no effect on cord formation or cord morphology. The testes from trkC and NT3 knockout mice were examined to determine if there were any morphological differences in the testis. NT3 knockouts appeared to have normal cord morphology in E15 and E17 testis. TrkC knockout mice also had normal cord morphology in E14 and P0 testis. Both NT3 and trkC knockout-mice testis had less interstitial area than wild-type controls. In addition, the trkC knockout mice have an increased number of cells expressing p75LNGFR within the cords when compared to controls or NT3 knockout mice. Combined observations suggest compensation between the different neurotropin ligands, receptors, and/or possibly different growth factors for this critical biological process. In summary, results suggest a novel nonneuronal role for neurotropins in the process of cord formation during embryonic rat testis development. The hypothesis developed is that neurotropins are involved in the progression of male sex differentiation and are critical for the induction of embryonic testis cord formation.

Animals↗
PubMed1995

Signs of aging are apparent in the testis interstitium of Sprague Dawley rats at 6 months of age.

The present study investigated the effects of aging in the testis interstitium in Sprague Dawley rats. Rats of 3, 6 and 24 months of age were used. Testes of rats (n = 5) were fixed by whole body perfusion using a fixative containing 2.5% glutaraldehyde in cacodylate buffer, processed and embedded in eponaraldite. Using 1 microns sections stained with methylene blue, qualitative and quantitative morphological studies were performed. Purified Leydig cell preparations, obtained by collagenase digestion followed by elutriation and density gradient centrifugation, were used to determine luteinizing hormone (LH; 100 ng/ml) stimulated testosterone secretory capacity per Leydig cell in vitro. Testosterone levels in the incubation medium, and testosterone and luteinizing hormone levels in serum of these three groups of rats were determined via radioimmunoassay. Morphological studies revealed that Leydig cells were more abundant in the testis interstitium at 6 and 24 months when compared to 3 months. Moreover, collagen fiber bundles were more frequently observed in the testis interstitium at older ages. Blood vessels of the testis interstitium in 24-month-old rats frequently showed partial and complete occlusion of their lumen and thickening of vessel walls. This feature was also present at 6 months, but less frequently. The results of the stereological studies revealed that the volumes of seminiferous tubules, interstitium and Leydig cells per testis was significantly higher (P < 0.05), at 6 and 24 months of age than those at 3 months. Moreover, volume of macrophages per testis was observed to be significantly higher (P < 0.05) at 6 months when compared to 3 and 24 months, and volume of connective tissue cells per testis was observed to be significantly lower (P < 0.05) at 6 and 24 months when compared to 3 months of age. No significant difference (P > 0.05) was observed for the volume of lymphatic space per testis in the three age groups studied. Volume of interstitial blood vessels per testis was not significantly different at 3 and 6 months of age, but a significantly greater (P < 0.05) volume was observed at 24 months. However, at 6 and 24 months, only 71% and 31% of the total blood vessel volumes respectively had completely open lumen in them; the rest of the blood vessels were either partially (12.5% at 6 months and 17% at 24 months) or completely (16.5% at 6 months and 52% at 24 months) occluded. The number of Leydig cells per testis was doubled at 6 and 24 months of age compared to 3 months. The average volume of a Leydig cell was not significantly different between 3 and 6 months of age, however, at 24 months a significantly lower (P < 0.05) value was observed. LH stimulated testosterone secretory capacity per Leydig cell in vitro was reduced by 50% at 6 months of age compared to 3 months; a further significant (P < 0.05) reduction was observed at 24 months. Serum testosterone and LH levels were not significantly different between 3 and 6 months of age but at 24 months a significantly lower (P < 0.05) value was observed for both of these hormones. In summary, the present study demonstrated many changes in the components of the testis interstitium in the aged Sprague Dawley rat. Modifications in the blood vessels and the occurrence of abundant collagen fibers in the interstitial space could possibly contribute to the reduced testosterone secretory capacity per Leydig cell with advancing in age. The observed Leydig cell hyperplasia could be suggested as a compensatory effort to maintain the normal androgen status of the aged rat, which is rather successful at 6 months but unsuccessful at 24 months. This investigation further revealed that these characteristic changes in the aged testis interstitium at 24 months are also present to some extent at 6 months of age in Sprague Dawley rats, suggesting that aging of the testis in this strain of rats commences early in life.

Aging↗
PubMedDate not supplied

Actions of the endocrine disruptor methoxychlor and its estrogenic metabolite on in vitro embryonic rat seminiferous cord formation and perinatal testis growth.

The current study examines the actions of methoxychlor and its estrogenic metabolite, 2, 2-bis-(p-hydroxyphenyl)-1, 1, 1-trichloroethane (HPTE), on seminiferous cord formation and growth of the developing rat testis. The developing testis in the embryonic and early postnatal period is likely more sensitive to hormonally active agents than at later stages of development. Embryonic day 13 (E13) testis organ cultures were treated with either 0.2, 2, or 20 microM methoxychlor or 1, 3, 6, 15, 30, or 60 microM HPTE to examine effects on cord formation. No concentration of methoxychlor completely inhibited cord formation. However, cord formation was abnormal with the presence of a reduced number of cords and appearance of "swollen" cords at the 2 and 20 microM concentrations of methoxychlor. The swollen cords were due to an increase in the number of cells in a cord cross section and reduction of interstitial cell numbers between cords. Treatment of embryonic day 13 (E13) testes with HPTE caused abnormal cord formation at the 3 microM and 6 microM concentrations, and completely inhibited cord formation at the 15, 30, and 60 microM concentrations. In addition to the estrogenic metabolite HTPE, methoxychlor can also be metabolized into anti-androgenic compounds. Therefore, to determine the spectrum of potential actions of methoxychlor on testis development, different concentrations of estradiol, testosterone, and an anti-androgen (flutamide) were utilized to determine their effects on E13 testis organ culture morphology. Estradiol (1 microM) and flutamide (0.1microM) both inhibited seminiferous cord formation in E13 testis organ cultures. Therefore, methoxychlor may be acting through the androgen and/or estrogen receptors to elicit its actions on seminiferous cord formation. Reverse transcription polymerase chain reaction (PCR) (RT-PCR) confirmed the presence of estrogen receptor alpha (ERalpha) mRNA from embryonic day 14 (E14) through postnatal day 5 (P5) while estrogen receptor beta (ERbeta) mRNA did not appear until approximately E16 of testis development. Androgen receptor (AR) expression was present from E14 through P5 of testis development, but at apparently reduced levels at E14 and E16. Immunohistochemical analysis localized ERalpha to the cells of the seminiferous cords at E14 though P5 while ERbeta was present in cells of the interstitium at E16 and P0. Androgen receptor was localized to germ and interstitial cells. The effects of methoxychlor, HPTE, estradiol, and testosterone on cell growth of perinatal testes was determined with a thymidine incorporation assay in postnatal day zero (P0) testis cell cultures. Methoxychlor (0.002, 0.02, and 0.2 microM) and HPTE (2 and 20 microM) stimulated thymidine incorporation in P0 testis cell cultures in a similar manner to estradiol (0.01, 0.1, and 1 microM). In addition, testosterone (0.1 microM) also stimulated thymidine incorporation in P0 testis cultures. Observations suggest that methoxychlor and its metabolite HPTE can alter normal embryonic testis development and growth. The actions of methoxychlor and HPTE are likely mediated in part through the steroid receptors confirmed to be present in the developing testis.

Animals↗
PubMed1988

Evidence for active immunological regulation in prevention of testicular autoimmune disease independent of the blood-testis barrier.

It has long been considered that autoimmune disease of the testis is prevented by sequestration of testis-specific autoantigens on germ cells behind the blood-testis (BT) barrier. However, we now have evidence that not all such antigens are sequestered. Some appear to reside on germ cells in the basal compartment of the seminiferous tubule where they are accessible to antibodies and to circulating activated T cells. Mice immunized with syngeneic testis homogenate are found to have immunoglobulin G (IgG) bound to cells in the basal compartment before onset of orchitis. This IgG is absorbed from circulation by the testis and, therefore, found only in the serum of mice orchiectomized before immunization. When the IgG is eluted from the testis, it is found to react preferentially with testicular cells enriched in preleptotene spermatocytes. T cells from mice immunized with testis can be transferred to naive syngeneic mice where they infiltrate the testis to cause orchitis. This implies that the BT barrier does not need to be breached directly for specific T cells to have access to testicular autoantigens on antigen presenting cells. Thus, active systemic and/or local immunoregulatory mechanisms must operate to prevent testicular autoimmune disease. These mechanisms may operate at the level of suppressor T cells, nonspecific suppression in the local environment of the testis, antigen presentation in the testis, or lymphocyte trafficking in the testis. These mechanisms probably operate only on the afferent limb of the immune response since they are overridden and orchitis occurs once testis-specific activated T cells are generated.

Animals↗
PubMed1975

Androgen binding protein as a biochemical marker of formation of the blood-testis barrier.

Androgen binding protein (ABP) was measured during postnatal development in normal and irradiated rats to determine whether development of a blood-testis barrier and formation of a continuous lumen from testis to epididymis is correlated with entry of ABP into the caput epididymis. ABP is found in normal testis as early as 14 days postnatally (0.2 pmol/mg), at which time no blood-testis barrier is observed by the peroxidase perfusion technique. Previous findings have shown a close correlation of blood-testis barrier development and lumen formation. Indeed, ABP is not detectable in the epididymis until 18-20 days of age (1.0 pmol/mg) at which time blood-testis barrier formation and lumen development is complete. Whole body irradiation (125 rads) of pregnant rats at 19-20 days of gestation produces male offspring with seminiferous tubules remarkably free of germinal epithelium and containing essentially only Sertoli cells. These Sertoli cell-enriched (SCE) testes produce normal amounts of ABP between 14 and 21 days postnatally. However, between 21 and 30 days of age the specific activity of ABP is significantly higher in the SCE tests (2.8 pmol/mg protein) than in normal testis (0.5 pmol/mg protein). In the SCE testis neither blood-testis barrier development nor lumen formation are complete until 30 days of age, at which time ABP is first detectable in epididymis of the irradiated rat. Thereafter there is a gradual decline of ABP in the SCE testis-and a dramatic increase in the epididymis. NIH-FSH-S-10 (200 mug/rat) injected SC into 14-day-old normal rats stimulated ABP in the testis from control levels of 0.15 pmol/mg to 1.46 pmol/mg within 4 h after injection. However, no ABP was detectable in the epididymis of either the control or the FSH-stimulated rats. These findings suggest that entry of ABP into caput epididymis is an index of blood-testis barrier formation and lumen development.

Androgens↗
PubMed1998

Mode of migration of normal lymphocytes inside murine testis.

BACKGROUND: Previous studies have shown that in murine experimental autoimmune orchitis (EAO), lymphocytes preferably infiltrate into (1) the testicular capsule near the rete testis, (2) the subcapsular interstitium away from the rete testis, and (3) the interstitium surrounding the tubuli recti and rete testis. Therefore, these three sites might provide tissue environments in which specific lymphocytes can easily gain access to testicular autoantigens. However, there is another possibility that infiltrating lymphocytes in the testis spontaneously accumulate at these three sites via the lymphatic flow inside this organ during EAO. METHODS: To examine this possibility, normal lymphocytes were locally injected into the peripheral testis regions of recipient mice. Testes were then collected at various times for investigating the chronological pattern of lymphocytic migration inside the testes at a light microscopic level. RESULTS: The injected lymphocytes first stayed in the lymphatic space around the seminiferous tubules and then moved to the subcapsular lymphatic space away from the rete testis. The lymphocytes accumulated under the testicular capsule and then gradually infiltrated into the adjacent capsular tissue. In the capsule, the cells surrounded the arteriolae and then accumulated in the capsular tissue near the rete testis. Thereafter, the cells finally left the testes through the lymphatics running in the spermatic cords. In the course of the lymphocytic drainage, it was noted that the injected lymphocytes appeared not to pass through the testicular interstitium around the tubuli recti and rete testis. CONCLUSIONS: The regional distributions of the testicular lymphocytes imply that the lymphatic flow in the testis may somewhat influence murine EAO pathology characterized by lymphocytic accumulation in (1) the testicular capsule near the rete testis and (2) the subcapsular interstitium away from the rete testis. However, the pathology exhibiting lymphocytic accumulation in (3) the interstitium around the tubuli recti and rete testis is independent on the intratesticular lymph flow.

Animals↗