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T T Turner

Publications and source records attributed to T T Turner.

At least 73 records · Page 4Linked to original sources
PubMed1982

Sperm motility-inhibiting factor in rat epididymis.

Rat spermatozoa collected by micropuncture from the cauda epididymidis are immotile when diluted in cell-free cauda epididymidal fluid but are vigorously motile when diluted in 0.154 M NaCl. Removal of proteins from cauda fluid by heat precipitation or enzymatic digestion reduces the ability of cauda fluid to keep cauda sperm immotile. Cauda sperm diluted in trypsin-treated cauda fluid have motility initiation scores that are not significantly different (P less than 0.05) from cauda sperm motility scores after dilution in 0.154 M NaCl. Cell-free lumen fluids from the proximal epididymis have a reduced ability to enforce quiesence on cauda spermatozoa, and rete testis fluid does not keep cauda sperm immotile. However, concentrated rete testis fluid does prevent the initiation of motility. It is proposed that a proteinaceous factor, possibly of testicular origin, is important in preventing the initiation of motility while sperm reside in the distal reproductive tract of the male rat.

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PubMed1981

Influence of surgically induced varicocele on testicular blood flow, temperature, and histology in adult rats and dogs.

Varicocele had been repeatedly implicated as a cause of infertility in selected men, although neither a causal relationship nor a mechanism has been documented. The purpose of this investigation was to create a varicocele model in animals and to study the subsequent alterations in testicular physiology. Secondary dilatation of the left internal spermatic vein was achieved either by partial ligation of the left renal vein in rats and dogs or by surgical destruction of the valve of the left testicular vein in a second group of dogs. 1 mo after partial ligation in the rats and 3 mo after partial ligation or valve destruction in the dogs, testicular blood flow was measured using Strontium 85 (SR-85)-labeled microspheres (15 +/- 1.1 micrometer). Intratesticular temperature was measured with a Bailey needle probe thermometer and biopsies were obtained for histologic sections. Mean testicular blood flow in milliliters per minute per 100 g was significantly greater in the partially ligated rats; right testis control 26 +/- 2, left testis control 24 +/- 2 compared to right testis experimental 35 +/- 3, left testis experimental 35 +/- 4 (p less than 0.02). Dogs undergoing either partial vein ligation or valve destruction showed similar increases in mean testicular blood flow; right testis control 8 +/- 1, left testis control 8 +/- 1 vs. right testis experimental 16 +/- 3, left testis experimental 18 +/- 4 (p less than 0.01). The mean difference between intratesticular and intraperitoneal temperature in control rats was significantly higher (4.02 +/- 0.25 degrees C right testis, 3.77 +/- 0.14 degrees C left testis), than rats who underwent partial vein ligation (right testis 2.14 +/- 0.09 degrees C, left testis 2.34 +/- 0.12 degrees C) (p less than 0.001). Control dogs also had a significantly higher mean difference between intratesticular and rectal temperatures; (right testis control 3.61 +/- 0.42 degrees C, left testis control 3.60 +/- 0.40 degrees C) than the partially ligated or valve destruction dogs (right testis 2.31 +/- 0.17 degrees C, left testis 2.67 +/- 0.32 degrees C) (p less than 0.05). In addition, histologic evaluation revealed abnormalities in spermatogenesis in some of the animals. Thus, venous dilatation secondary to partial vein ligation or testicular vein valve obliteration is followed by large bilateral increases in testicular blood flow in these two species. A consequence of this increased flow is an elevation in bilateral testicular temperature, which it is postulated, leads to impaired spermatogenesis in some of the animals. In selected men varicocele may impair spermatogenesis by a similar physiologic mechanism.

Animals↗
PubMed1981

Effect of oestradiol valerate on the rat blood--testis and blood--epididymal barriers to [3H]inulin.

Micropuncture samples were taken from rats treated with 2.9 mg oestradiol valerate/day for 14 days, sham injected or untreated. Oestradiol valerate treatment reduced testicular weight and serum testosterone concentrations (P less than 0.05), but did not alter the movement of [3H]inulin into seminiferous tubules or those of the cauda epididymidis. [3H]Inulin concentrations in the seminiferous tubule fluids were always less than 8% of blood isotope concentrations, and those in cauda epididymal tubuule fluid were always less than 5% of blood isotope concentrations. It was concluded that the maintenance of the anatomical component of the blood--testis and blood--epididymal barriers (cell--cell tight junctions) is not androgen-dependent.

Animals↗
PubMed1981

Cyclophosphamide, vincristine, and the blood testis barrier.

The blood testis barrier has been implicated in the pathogenesis of testicular relapse of childhood acute leukemia by forming a "sanctuary site" for leukemic cells. Experiments were conducted to test the transport of carbon 14 cyclophosphamide and tritiated vincristine across the blood testis barrier. Both cyclophosphamide and vincristine crossed the blood testis barrier. However, other factors such as the transport of immunoglobins and leukocytes across the blood testis barrier may interact in the pathogenesis of leukemic testicular relapse.

Animals↗
PubMed1981

The blood epididymal barrier to [3H]-inulin in intact and vasectomized hamsters.

The net transport of [3H]-inulin into the fluids of the hamster seminiferous and caput, corpus, and cauda epididymal tubules was examined in both intact animals and those vasectomized 10 months previously. Mean isotope concentrations in reproductive tract tubule fluids did not exceeded 10 per cent of blood plasma isotope concentrations during the experiment. There were no significant differences in net transport of [3H]-inulin into any of the tubule fluids sampled. Ten months after vasectomy, the seminiferous tubule, and all regions of the epididymal tubule retain the capacity to exclude [3H]-insulin. Thus in the hamster 10 months after vasectomy, the blood testis and blood epididymal barriers to inulin are intact.

Animals↗
PubMed1980

[3H]3-O-methyl-D-glucose transport from blood into the lumina of the seminiferous and epididymal tubules in intact and vasectomized hamsters.

The investigation demonstrated a restriction of [3H]3-O-methyl-D-glucose ([3H]3-OMG) net transport into seminiferous tubule fluid. Net transport of [3H]3-OMG into the cauda epididymidal tubule was even more limited. By 4 months after vasectomy, there was no statistical difference in the net transport of the isotope into the seminiferous tubule fluid, but there was a significant increase in net transport into cauda epididymidal fluid. These results demonstrate that the blood-epididymal barrier can be even more restrictive to molecular transport than the blood-testis barrier and that vasectomy can have subtle effects on characteristics of molecular transport in the cauda epididymidis.

Animals↗
PubMed1979

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↗
PubMed1978

The blood-testis barrier: a morphologic or physiologic phenomenon?

Blood urea is concentrated in rat seminiferous tubule fluid. Data are presented that provide strong evidence that this urea movement is dependent on active sodium transport. In contrast, in the hamster blood urea is excluded partially from the seminiferous tubule. This may be caused by transport of urea from the lumen to the blood rather than secondary to the morphologic blood, testis barrier at the Sertoli to Sertoli cell tight junctions.

Animals↗
PubMed1978

The effects of vasectomy on the movement of 14C-urea in the seminiferous tubule of the hamster.

14C-urea entry into the hamster seminiferous tubule (SNT) and cauda epididymidal tubule was observed in intact males and in animals vasectomized for 2 weeks and for 4 months. 14C-urea entry rate and plateau level were significantly increased 4 months postvasectomy. 14C-urea entry into the cauda epididymidis was significantly altered 2 weeks postvasectomy. 2, 4,-dinitrophenol significantly increased 14C-urea concentration in the SNT. This is compatible with the presence of an outward directed energy dependent movement of urea in the hamster SNT. Increasing 14C-urea concentrations in the postvasectomy SNT may be attributable to a failure or inhibition of this physiologic activity.

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