Fluctuations in Rat Testicular Interstitial Oxygen Tensions Are Linked to Testicular Vasomotion: Persistence after Repair of Torsion1

Lysiak, Jeffrey J.; Nguyen, Quoc An T.; Turner, Terry T.

doi:10.1095/biolreprod63.5.1383

Cited by 62 publications

(57 citation statements)

References 25 publications

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“…An in vivo model is preferred to understand testicular physiology, as there are autoprotective mechanisms against low O 2 tension in the testis (Elshaari et al 2012) and natural antioxidant systems (Aitken and Roman 2008;Reyes et al 2012) that are difficult or impossible to replicate in an in vitro model. Furthermore, under heat stress, testicular vasomotion (rhythmic tone variation in blood vessels) is greatly suppressed (Setchell et al 1995) which can impair testicular function (Lysiak et al 2000;Aalkjaer et al 2011). …”

Section: Discussionmentioning

confidence: 99%

Hyperthermia and not hypoxia may reduce sperm motility and morphology following testicular hyperthermia

Kastelic¹,

Wilde²,

Rizzoto³

et al. 2017

Vet. Med.

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ABSTRACT:The mammalian testis typically operates on the brink of hypoxia; the long-standing dogma is that increased testicular temperature increases metabolism, but blood flow is unaffected and the resulting hypoxia reduces sperm motility and morphology. In rats and mice, oxygen (O 2 ) content of inspired air affected O 2 content of testes, enabling the latter to range from approximately 50 to more than 200% of physiologic concentrations. A ram model was used to test the hypotheses that hypoxia would disrupt sperm motility and morphology and that hyperoxia would prevent hyperthermia-induced reductions in sperm motility and morphology. Eighteen Canadian Arcott rams (approximately 10 months old) were used in a 2 × 3 factorial, with factors being scrotal insulation (insulated or not insulated) and O 2 concentrations in inspired air (14, 21 or 85%). Six rams, three with and three without scrotal insulation, were placed in each of three enclosed areas for 30 h to expose them to their respective oxygen concentrations, with scrotal insulation removed at the end of the exposure. Semen was collected by electro-ejaculation twice before insulation, bi-weekly for four weeks starting one week after exposures, and then once weekly for two weeks. There were effects of insulation, time and an insulation × time interaction for motile sperm and sperm that had normal morphology or head or midpiece defects (P < 0.01 for each). Sperm motility and morphology exhibited alterations between approximately two and five weeks after insulation, with mean progressively motile and morphologically normal sperm decreasing from approximately 55 to 35% and from 80 to 30%, respectively, and with head and midpiece defects increasing from approximately 3 to 50% and from 10 to 20% (P < 0.05 for each). The hypotheses that hypoxia would disrupt sperm quality and production, whereas hyperoxia would prevent hyperthermia-induced reductions in sperm quality and production, were not supported. This is apparently the first report that heat-stress induced damage to sperm was due to increased temperature per se and not testicular hypoxia, calling into question a long-standing paradigm.

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Section: Discussionmentioning

confidence: 99%

Hyperthermia and not hypoxia may reduce sperm motility and morphology following testicular hyperthermia

Kastelic¹,

Wilde²,

Rizzoto³

et al. 2017

Vet. Med.

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show abstract

“…However, blood vessels are located exclusively between the tubules, and oxygen reaches the lumen of the seminiferous tubules only by diffusion. The seminiferous epithelium was speculated to operate on the verge of hypoxia because the testicular PO 2 is relatively low, oxygen extraction is highly related to the metabolic demands of spermatogenesis, oxygen diffusion distance is comparatively long, and the testis has little capacity to increase total blood flow (Lysiak et al 2000). Furthermore, exposure to hypoxia results in distribution of blood flow to the vital organs including brain and heart, and decrease in testicular blood flow.…”

Section: Discussionmentioning

confidence: 99%

Hypobaric hypoxia causes deleterious effects on spermatogenesis in rats

Liao¹,

Cai²,

Chen³

et al. 2010

Reproduction

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The study was conducted to explore the effects of hypobaric hypoxia on spermatogenesis in rats. Adult male Wistar rats were randomly divided into four groups: three hypoxia-exposed groups and one normoxic control group. Rats in the normoxic control group were raised at an altitude of 300 m, while rats in the 5-, 15-, and 30-day hypoxic groups were raised in a hypobaric chamber simulating a high altitude of 5000 m for 5, 15, and 30 days respectively. Flow cytometry was used to detect the DNA content of testicular spermatogenic cells in rats. The apoptosis of germ cells in testis was analyzed by using TUNEL assay. Spermatogenesis was also evaluated by morphology. Flow cytometry analysis revealed that 5-30 days of hypobaric hypoxia exposure significantly reduced the percentage of tetraploid cell population in rat testis. After rats were exposed to hypobaric hypoxia for 30 days, the ratio of haploid and diploid cell populations in testis reduced significantly. Seminiferous tubules with apoptotic germ cell increased after exposure to hypoxia. Most apoptotic germ cells were spermatogonia and spermatocytes. Hypoxia also caused decrease of cellularity of seminiferous epithelium, degeneration and sloughing of seminiferous epithelial cells occasionally. The data suggest that hypobaric hypoxia inhibits the spermatogenesis in rats. Decrease of tetraploid spermatogenic cells (primary spermatocytes) induced by hypoxia is an important approach to suppress spermatogenesis. The apoptosis of primary spermatocytes and spermatogonia may contribute to the loss of tetraploid cell populations.

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“…However, blood vessels are located exclusively between the tubules, and oxygen reaches the lumen of the seminiferous tubules only by diffusion. The seminiferous epithelium was speculated to operate on the verge of hypoxia because the testicular partial pressure of oxygen (PO 2 ) is relatively low, oxygen extraction is highly related to the metabolic demands of spermatogenesis, oxygen diffusion distance is comparatively long, and the testis has little capacity to increase total blood flow (Lysiak et al 2000). Furthermore, exposure to hypoxia results in redistribution of blood flow to the vital organs including brain and heart and decrease in testicular blood flow, Koskinen et al (2000) reported that breathing 10 % O 2 / 90 % N 2 resulted in a 24 % decrease in testicular blood flow, but a 23 % increase in ce- rebral blood flow.…”

Section: Discussionmentioning

confidence: 99%

Reversible Effect of High Altitude on Rat Testis Morphology and Spermatogenesis: Histological and Ultrastructural Study

et al. 2016

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SUMMARY:The study was carried out at two different altitudes in the southern region of Saudi Arabia: Abha, 2,800 meters above sea level, the high altitude (HA) area and Jazan, 40 meters above sea level the low altitude (LA) area. Following exposure to high altitude, testes of rats revealed various types of atrophy and degeneration in the seminiferous tubules and in the interstitial tissue. There was detachment of the basal laminae of the tubules and a profound decrease in cellularity. When rats were brought back to their habitat (LA) and later examined, many tubules showed normal population of cells including spermatids and spermatozoa. Well-arranged epithelium was seen in most of the seminiferous tubules of these animals, normal interstitial space and no detachment of the basal lamina. Apparently complete recovery had been achieved ultrastructurally, in hypoxic group; some spermatogenic cells lost their normal architecture, being irregular in shape with some features of necrosis, such as shrinkage and pyknotic nuclei characterized by chromatin condensation. Significant decrease in epithelial height was noticed in these animals (P <0.05). Also, the diameter of the tubules showed slight decrease with concomitant increase in interstitial spaces.

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Fluctuations in Rat Testicular Interstitial Oxygen Tensions Are Linked to Testicular Vasomotion: Persistence after Repair of Torsion1

Cited by 62 publications

References 25 publications

Hyperthermia and not hypoxia may reduce sperm motility and morphology following testicular hyperthermia

Hyperthermia and not hypoxia may reduce sperm motility and morphology following testicular hyperthermia

Hypobaric hypoxia causes deleterious effects on spermatogenesis in rats

Reversible Effect of High Altitude on Rat Testis Morphology and Spermatogenesis: Histological and Ultrastructural Study

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