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At least 19 recordsLinked to original sources

Blood-testis barrier: maintained function of inter-Sertoli cell junctions in experimental cryptorchidism in the rat, as judged by a simple lanthanum-immersion technique.

In order to elucidate the mechanisms behind the deleterious effects on the germinal epithelium of experimental cryptorchidism the hypothesis that a leaking blood-testis barrier is the cause of the damage was tested. The permeability of the specialized inter-Sertoli cell junctions to lanthanum after experimental cryptorchidism for 0.5 to 12 days was studied in the rat. In none of the time periods studied lanthanum had penetrated beyond the inter-Sertoli cell junctions. A simple lanthanum immersion technique was used. Testes of 15-days old rats (before the development of the barrier) were used as a positive control of the method, and in these testes lanthanum had penetrated up to the future lumen.

Blood-Testis Barrier↗

Steroid entry into rete testis fluid and the blood-testis barrier.

Evidence that steroids enter rete testis fluid (RTF) from the blood at varying rates was obtained during i.v. infusions into rats. Testosterone and dehydroepiandrosterone were readily transferred into the fluid, whereas cholesterol was excluded. Between these extremes, the appearance of radioactivity in the RTF suggested the following order of entry rate: progesterone greater than pregnenolone greater than 5-alpha-reduced androgens greater than oestrogens greater than corticosteroids. Preliminary identification of metabolites in RTF and blood suggested that testosterone and dehydroepiandrosterone were transferred largely unchanged. Androstenedione and progesterone, however, were largely metabolized during transfer into the RTF, the former being transformed to testosterone. The results are used to discuss the nature of the blood-testis barrier to steroids and the source of androgens in the RTF.

Androgens↗

Effects of vasectomy on the blood-testis barrier of the hamster.

The effects of vasectomy on the blood-testis and blood-epididymal barriers to 3H2O, [3H]inulin, and [14C]urea were examined by study of the radioactivity appearing in micropuncture samples of fluids from the seminiferous tubules and cauda epididymidis. By 4 months after vasectomy, there were changes in the blood-seminiferous tubule barrier to [3H]water and [14C]urea (increased entry) and in the blood-epididymal barrier to [3H]water and [3H]inulin (increased entry) and to [14C]urea (decreased entry). These subtle changes could have an impact on spermatogenesis and/or sperm maturation after vasectomy.

Animals↗

Observations on the inter-relationships of Sertoli cells at the level of the blood- testis barrier: evidence for formation and resorption of Sertoli-Sertoli tubulobulbar complexes during the spermatogenic cycle of the rat.

Structures termed tubulobulbar complexes are known to be formed by adjoining Sertoli cells at the level of the blood-testis barrier (Russell and Clermont, '76). Here, long (2-4 micrometer) tubular evaginations of one Sertoli cell, which end in bulbous dilations, are seen in corresponding invaginations of a neighboring Sertoli cell. In most regions of the tubular and bulbous portions of the complex, the Sertoli plasma membranes were found to be separated by a 4-5-nm intercellular space, but in some areas the membranes converged to form tight and gap junctions. The numbers, distribution and properties of tubulobulbar complexes were studied in relation to the cycle of the seminiferous epithelium. From the data obtained it was concluded that tubulobulbar complexes develop and undergo regressive changes during the spermatogenic cycle. Most complexes arise during the early stages of the cycle (Stages II-V) and develop large bulbous endings. Developing tubulobulbar complexes consist of short evaginations of one Sertoli cell which face a bristle-coated pit of the opposing Sertoli cell. At midcycle (Stages VI-VII) most show regressive changes and are eventually resorbed as a consequence of the action of nearby Sertoli lysosomes. Once resorbed, the probability of seeing a tubulobulbar complex in thin sections decreases from 4- to 8-fold. The few tubulobulbar complexes which remain past this period (Stages VII-XIV-I) usually lack bulbous endings and are fequently seen above type A spermatogonia. The data suggest that small fragments of cytoplasm and plasma membrane (including junctional surfaces) are lost from one Sertoli cell as a result of the degradative processes occurring in a neighboring Sertoli cell. Tubulobulbar resorption is discussed in relation to the impending breakdown of the blood-testis barrier above spermatocytes as these cells move upward. The possible significance of the cyclic resorption of tight and gap junctional sites between Sertoli cells is also discussed.

Acid Phosphatase↗

Testicular lesions of coprine and benzcoprine.

The effect on the testis of the disulfiram-like compounds benzcoprine (N-[1-ethoxycyclopropyl] benzamide) and coprine (N5-[1-hydroxycyclopropyl]-L-glutamine) was studied in rats and dogs. Severe degeneration of the seminiferous epithelium was induced in rats by subacute oral administration of each compound. 60 days after termination of treatment with benzcoprine most seminiferous tubules contained only occasional spermatogonia and the testicular weight was markedly decreased. The blood-testis barrier was unaffected in the benzcoprine-treated rats as judged by a lanthanum tracer technique. In dogs, oral administration of benzcoprine for 1 month caused impaired spermatogenesis, degeneration of germ cells and a decrease in the testicular weight. The results indicate that both compounds act directly on the germ cells. The effect is similar to that of alkylating compounds. Other effects of benzcoprine and coprine (bone marrow depression, lymphocytopenia, positive Ames test in organisms sensitive to base-pair substitution) are well-known properties of alkylating agents. In conclusion benzcoprine and coprine were found to cause severe changes in the testis in rats and dogs, probably due to a direct effect on the germ cells.

Animals↗

[Treatment of relapses in juvenile acute lymphoblastic leukemia].

Recurrence of childhood acute lymphoblastic leukemia occurs in about 30-50% and indicates irresistable progression of the disease. While systemic (= hematologic) relapse is due to drug resistance of leukemic cells, pharmacologic barriers may be responsible for local relapses as meningeal involvement, leukemic ophthalmopathy or testicular infiltration. L-asparginase seems to be an important component of drug combinations for re-induction therapy for systemic relapse. Following reinduction therapy modification of continuation therapy is necessary. Local relapses require local treatment, i.e. radiotherapy and e.g. intrathecal drug application. Local relapse is almost always followed by hematologic relapse. Therefore, intensification of systemic therapy is also recommended. Prevention of these relapses is much more important and probably more successful than treatment. Therefore, initial therapy should include preventive measures for pharmacologic sanctuaries.

Asparaginase↗

The effect of vasectomy on the testes of inbred Lewis rats.

By 3 months after surgery, testicular weights were 12-14% below control values in a large series of vasectomized rats of the inbred Lewis strain. Testicular sperm concentrations in the vasectomized rats were 25-29% below those in the sham-operated animals. Although modest in magnitude, these differences were highly significant (P less than 0.001). Histometric analysis of testes from a smaller series of vasectomized Lewis rats revealed various proportions of abnormal seminiferous tubules. The degenerative changes included reduction in tubule diameter, fusion of spermatids, and depletion of advanced germinal elements. In the most severely affected tubules, leakiness of the blood-testis barrier was indicated by penetration of lanthanum through Sertoli-cell tight junctions.

Animals↗

Hormonal regulation of testicular descent: experimental and clinical observations.

Hormonal regulation of testicular descent has been investigated. Based on experimental studies using the rat and on a review of clinical material it has been determined that testicular descent is an androgen-mediated event directly under the regulation of pituitary gonadotropin. Furthermore, the active androgenic metabolite involved in this process appears to be dihydrotestosterone, which is synthesized by the testis and must be present in high local concentrations to be effective. In addition to these hormonal requirements the anatomy of the inguinal canal must provide unimpeded migration of the testis into the scrotum. Any imbalance or anomaly of these prerequisites may lead to cryptorchidism.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗

The effect of temperature on the potential difference and input resistance of rat seminiferous tubules.

1. The p.d. of rat seminiferous tubules was 5.86 +/- 0.15 mV, lumen negative, at 33 degrees C and varied linearly with temperature between 24 and 37 degrees C, exhibiting an apparent Q(10) (25-35 degrees C) of 2.0 with a slope of 0.43 mV/ degrees C. Exposing testes to a temperature of 37-43 degrees C resulted in an initial hyperpolarization followed by depolarization of the tubules. These changes were more rapid in testes exposed to 41-43 degrees C than in testes exposed to 37-39 degrees C.2. The R(in) of seminiferous tubules was 198 +/- 7.8 kOmega at a testis temperature of 33 degrees C. The R(in) decreased when testes were maintained at 37 and 41 degrees C, the rate of decrease being similar to the rate of depolarization.3. Exposing testes to deep body temperature by unilateral surgical cryptorchidism caused a reduction of 30 and 64% in tubular p.d. and R(in) respectively when measured 24 hr after surgery. Exposure to deep body temperature for up to 4 days did not cause any further change in either parameter.4. There was no evidence that lanthanum penetrated through the Sertoli cell tight junctions after exposing testes to 41 degrees C for up to 30 min.5. The results indicate that the seminiferous tubule p.d. is maintained by a temperature-sensitive, cellular mechanism. Exposing testes to deep body temperature or above depolarized the tubules and increased their permeability.

Animals↗

[Ultrastructure of Sertoli cells of the human testis in agenesis of the vas deferens].

Ten testicular biopsies from adult males with agenesis of the vas deferens have been investigated with light and electron microscopy. The ultrastructural study of SERTOLI cells has demonstrated that: (a) the junctions between SERTOLI cells and between SERTOLI and germinal cells retain their normal ultrastructural features. (b) Lanthanum permeates SERTOLI cells tight junctions, but its diffusion towards the adluminal compartment is prevented. (c) SERTOLI cells present unusual amounts of cytoplasmic inclusions, especially lipofuscin granules. A relationship between these inclusions and phagocytosis has not been demonstrated. (d) "Dark" SERTOLI cells which show alterations of their typical junctional complex have been frequently observed, although their frequency varies among the different patients. The results are discussed in relation to diagnostic significance of the ultrastructural study of testicular biopsies.

Blood-Testis Barrier↗