Biomedical subjects
T T Turner
Publications and source records attributed to T T Turner.
Postvasectomy alterations in protein synthesis and secretion in the rat caput epididymidis are not repaired after vasovasostomy.
Many men who have undergone vasectomy later request vasovasostomy. Unfortunately, significant numbers of these men remain infertile despite the reestablishment of patent ducts. This report examines the possibility that epididymal function remains compromised after vasovasostomy in the rat by examination of quantifiable, in vivo protein synthesis and secretion in the caput epididymidis. Rats were studied 30 days after vasectomy, 30 days after a vasovasostomy (which was performed 30 days after vasectomy), or after sham operations. Epididymal lumen fluids (LF) were collected by micropuncture after 3 hours' in vivo microperifusion of tubules with 35S-amino acids. Proteins were separated by 2-dimensional electrophoresis and were detected by Coomassie blue staining. Synthesized proteins in tubule extract and synthesized and secreted proteins in LF were detected by autoradiography and image analysis. Specific proteins that appeared to be affected by vasectomy-vasovasostomy were identified by internal sequence analysis. LF contained an average of 87 detectable proteins synthesized and secreted in the control caput. Nineteen of the most prominent LF proteins were selected for more focused study. The most prominent proteins were clusterin, cysteine-rich secretory protein (CRISP)-1, and epididymal retinoic acid-binding protein. Among these, CRISP-1 remained reduced in LF after vasovasostomy. Two more minor proteins that remained reduced after vasovasostomy were identified as prostaglandin D2 synthase and phosphatidylethanolamine-binding protein. All 3 of these proteins occur in the epididymides of multiple species and have been associated with sperm fertilizing capacity.
Hox transcription factors may play a role in regulating segmental function of the adult epididymis.
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Gonadotroph and Leydig cell responsiveness in the male rat. Effects of experimental left varicocele.
Previous experiments have found that experimental left-sided varicocele (ELV) in rats is associated with significant bilateral reductions in intratesticular testosterone concentrations. The current experiments were performed to determine the source of this endocrinopathy. Sensitivity and responsivity of Leydig cells and gonadotrophs were determined in control male rats and in those with ELV. Initially, dose-response relationships were determined for luteinizing hormone (LH) stimulation of testosterone secretion by Leydig cells and for luteinizing hormone releasing hormone (LHRH) stimulation of LH secretion by gonadotrophs. Maximally (ED100) and half-maximally (ED50) stimulating doses of LH and LHRH were selected from these studies and administered to sham-operated and ELV rats 30 days after the operation to induce ELV. Leydig cell and gonadotroph sensitivity (response to ED50) and responsivity (response to ED100) to LH and LHRH, respectively, were determined. Responsivity of Leydig cells in control and ELV rats was similar. Responsivity of gonadotrophs to LHRH was significantly suppressed in ELV animals, but the physiologic relevance of this singular finding is unclear. It is possible that the previously determined ELV-associated decrease in intratesticular testosterone concentrations is subsequent to a wash-out phenomenon that follows the increased testicular blood flow that also is known to be associated with ELV.
Fluid movement in the lumen of the rat epididymis: effect of vasectomy and subsequent vasovasostomy.
Intraluminal fluid movement rate was measured in four regions of the rat epididymis. The fastest flow occurred in the proximal caput epididymis (18.5 +/- 3.7 mm/hour) and the slowest in the distal cauda (2.5 +/- 0.5 mm/hour). Vasectomy significantly reduced caput fluid flow rates unless a sperm granuloma was present at the vasectomy site. Thirty days after vasovasostomy, caput fluid movement remained reduced in animals unless a granuloma was present. Failures of this or other aspects of epididymal biology to return to normal after vasovasostomy could play a role in the frequent infertility which persists after the operation.
Leydig cell function after experimental testicular torsion despite loss of spermatogenesis.
Little is known about specific testicular cell responses to periods of testicular torsion. In particular, the steroidogenic capacity of Leydig cells in the post-torsion testis is unknown. Male Sprague-Dawley rats (450-550 g) underwent no torsion (control) or a 720 degrees unilateral testicular torsion for either 0 (sham), or 1 or 2 Such torsions have previously been shown to cause progressive damage to the rat testis. One, 15, or 30 days after torsion repair all animals (n = 5-10/group) were prepared for testicular venipuncture and intravenous infusion of ovine luteinizing hormone (LH) via the femoral vein. Testicular venous blood was collected directly from the surface of the testis both 5 minutes prior to and 90 minutes after infusion of predetermined ED50 (0.1 microgram) or ED100 (0.5 microgram) doses of LH. Testicular venous serum (TVS) was assayed for testosterone (T) by radioimmunoassay. Control animal TVS T concentrations before LH infusion and 90 minutes after ED50 and ED100 LH stimulation were 103 +/- 25, 621 +/- 103, and 1,055 +/- 140 ng/ml, respectively. Testes having experienced a 1-hour torsion did not have a significantly (P < 0.05) reduced capacity to respond to ED50 and ED100 stimulation at either 15 and 30 days after the torsion. Testes having experienced a 2-hour torsion did have significantly reduced (P < 0.05) ED50 responses at both 1 hour and 30 days after torsion repair. More remarkably, significant steroidogenic reserve was still present in testes after torsion, which in previous studies had been shown to have permanent loss of spermatogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)
Testicular intravascular volume and microvessel mitotic activity: effect of experimental varicocele.
Testicular blood flow increases bilaterally in animals with experimental left varicocele (ELV). The present experiments were undertaken to determine if increases in testicular intravascular volume and capillary growth were potential contributors to this increase in flow. Testicular intravascular volume (microliters/g) was estimated by determining testicular vascular 125I-albumin space. Microvessel mitotic activity was estimated by examining 3H-thymidine incorporation into endothelial nuclei, as assayed by silver grain localization over microvessel endothelial nuclei after exposure of testes to 3H-thymidine in vivo. Testicular intravascular volume was 25-30 microliters/g testis in control testes and in ELV animals was increased an average of 9% and 28% in right and left testes, respectively. This increase was statistically significant (P < 0.05) on the left side only. Approximately 1.5-2.0% of testicular microvessel endothelial nuclei exhibited silver grain localization, and ELV was not associated with a change in these values in either right or left testis. Ancillarily, there was a modest but significant association between microvessel mitotic activity and mitotic activity in adjacent seminiferous tubules. It was concluded that bilateral increases in testicular blood flow after ELV are not uniquely the result of bilateral expansion of intravascular volume and growth of the testicular capillaries. It is speculated, however, that mitogenic factors from the seminiferous tubules potentially affect mitotic activity of the adjacent microvasculature.
On the epididymis and its role in the development of the fertile ejaculate.
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Endocrine and exocrine effects of testicular torsion in the prepubertal and adult rat.
Previous studies of experimental torsion have suggested that there may be important differences between the adult testis and the prepubertal testis in their responses to torsion, especially with regard to the potential for contralateral damage following unilateral testicular torsion. In the present study, adult Sprague-Dawley rats and prepubertal Sprague-Dawley rats (35 days of age) were subjected to unilateral 1-, 2-, and 4-hour periods of 720 degrees or 360 degrees testicular torsion. Ipsilateral and contralateral testes were examined 30 and 60 days after torsion repair for effects on testis weight, histology, and daily sperm production (DSP). Other animals were subjected to 1-/or 4-hour 720 degrees torsion, and testicular vein testosterone concentrations were determined 30 days later. In adult animals, 1-, 2-, and 4-hour 720 degrees torsion resulted in a significant decline in ipsilateral testis weight within 30 days. Endocrine and exocrine function were also clearly disrupted. In prepubertal animals, 1-hour 720 degrees torsion significantly reduced testis weight 60 days after surgery. Also, prepubertal DSP values and testicular vein testosterone concentrations were not significantly reduced from control values by 1-hour 720 degrees torsion when examined 30 days after surgery. Longer periods of 720 degrees torsion resulted in damage similar to that seen in the adult animals. Neither adult nor prepubertal animals regained any lost function when examined 60 days after insult. Torsion of 360 degrees induced no testicular injury in adult or prepubertal animals. Contralateral testes were not affected by degree or duration of torsion in either adult or prepubertal animals. These results suggest that the prepubertal testis may be more refractory to the effects of short periods of torsion than the adult. More importantly, these results demonstrate that ipsilateral torsion does not result in contralateral testicular damage in either adult or prepubertal animals.
Testicular capillary permeability: the movement of luteinizing hormone from the vascular to the interstitial compartment.
It has previously been shown in several species that pulses of luteinizing hormone (LH) in peripheral serum are followed within 10-20 minutes by pulses of testosterone. Whether or not LH pulses directly stimulate Leydig cells to produce the testosterone pulses would depend on the vascular permeability of LH within that physiologically relevant time. In the present experiments, the capillary permeability of the testicular microvasculature was characterized in adult rats, and the relative permeability to LH was determined. Adult male rats were prepared for in vivo micropuncture and testes were infused with 3H-water, 14C-urea, 14C-polyethylene glycol (PEG), and 3H-dextran directly into the testicular surface artery. Testicular interstitial fluid (TIF) and testicular venous plasma were collected at 5 minutes, 10 minutes, and 15 minutes after initiation of isotope infusion. Data were recorded as isotope concentration in TIF as a proportion of the isotope concentration in testicular venous plasma collected at the same time period. 3H-water movement into the TIF from blood was rapid reaching 50% of serum values within 15 minutes. 14C-PEG and 3H-dextran were largely excluded from the TIF, typically not exceeding 5-10% of serum concentrations. In subsequent experiments, 125I-LH was infused using the same protocol. 125I-LH concentrations in TIF were 3.6 +/- 2.0% of plasma concentrations 10 minutes after initiation of infusion. Preceding the 125I-LH infusion experiments with 5-day hypophysectomy or with LH pulses delivered either 10 minutes or 4 hours prior to the initiation of infusion did not alter the capillary permeability of 125I-LH. These data demonstrate the restricted availability of LH to the TIF. This implies that Leydig cells are not exposed to LH pulses through the TIF and raises the question whether LH pulses directly stimulate testosterone pulses.
Testicular microvascular blood flow: alteration after Leydig cell eradication and ischemia but not experimental varicocele.
Testicular microvascular blood flow is known to exhibit vasomotion, or pulsatile flow. In the present study we have used laser-Doppler flowmetry to study microvascular blood flow in the rat testis and to examine the response of the microvasculature to pharmacological stimulation and pathophysiological conditions. With a mean microvascular flow rate of 13.3 +/- 1.7 perfusion units (PU), the mean cycle amplitude was 3.4 +/- 0.6 PU, and the cycle frequency was 10.3 +/- 0.8 cycles per minute. Blood flow parameters did not differ between left and right testes, between scrotal testes and testes in a 35 degree C glass testicle receptacle, or among testicular regions. Perifusion of seminiferous tubules and their vasculature with 0.1 microgram/microliter epinephrine significantly reduced microvascular blood flow and eliminated vasomotion. Elimination of Leydig cells and intratesticular testosterone also eliminated vasomotion but did not significantly alter mean blood flow rates. Thirty days after imposition of experimental left varicocele (ELV) there were no significant changes in microvascular blood flow parameters. Testicular torsion of sufficient degree and duration to destroy spermatogenesis did not induce a change in mean microvascular blood flow rate 24 hours after repair of torsion, but testicular vasomotion was eliminated in the majority of animals. We conclude that microvascular flow is altered in some testicular pathologies and not in others. The mechanisms underlying changes in microvascular blood flow are at present unknown.
Interleukin-1 beta and tumor necrosis factor-alpha stimulate granulocyte colony-stimulating factor production by placental villous core mesenchymal cells.
OBJECTIVE: To test the hypothesis that interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) regulate granulocyte colony-stimulating factor (G-CSF) production by human placental villous core mesenchymal cells. METHODS: Villous core mesenchymal cells were isolated from placentas at 14-20 weeks' gestation and cultured in vitro. Cells were treated with IL-1 beta or TNF-alpha in dose-response and time-course studies. We measured G-CSF mRNA expression by Northern blot analysis and G-CSF protein production by enzyme-linked immunosorbent assay of the conditioned media. RESULTS: Unstimulated mesenchymal cells expressed negligible G-CSF. Steady-state G-CSF mRNA expression was maximal 3-6 hours after IL-1 beta treatment and 6-18 hours after TNF-alpha treatment. Each cytokine induced G-CSF protein production in dose-and time-dependent manners, with IL-1 beta more potent than TNF-alpha. The G-CSF mRNA expression and G-CSF protein production induced by the combination of both cytokines exceeded that induced by either cytokine alone. CONCLUSIONS: Interleukin-1 beta and TNF-alpha stimulate G-CSF production by placental villous core mesenchymal cells in vitro. These results identify a potential mechanism by which villous core mesenchymal cells mediate, in part, the placental response to these two cytokines.