Autoradiographic investigation of sperm transit through the male mouse genital tract after tritiated thymidine incorporation

Dadoune, J. P.; Alfonsi, Marie-Françoise

doi:10.1051/rnd:19840709

Cited by 19 publications

(18 citation statements)

References 11 publications

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“…Spermatozoa ejaculated 21 days after heating would have been pachytene and diplotene spermatocytes at the time of heating [42,43] and these cells have been previously reported to be seriously damaged by heat exposure [45,56,57] and this study. Apparently this damage can extend to an effect on the development of preimplantation embryos.…”

Section: Discussionmentioning

confidence: 97%

“…Spermatozoa ejaculated on 7 days after heating would have been in the epididymis at the time of heating [41,42]. Although the epididymis has previously been reported to be resistant to heat [43], heat stress could disturb epididymal maturation of the spermatozoa because heat stress has been shown to damage the chromatin structure of sperm in the epididymis of the mouse [44] and the bull [45].…”

Section: Discussionmentioning

confidence: 99%

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Effects of paternal heat stress on the in vivo development of preimplantation embryos in the mouse

Zhu

Setchell

2004

Reprod. Nutr. Dev.

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-The objective of this study was to examine the effect of paternal heat stress on the in vivo development of preimplantation embryos in the mouse. Synchronised B6CBF1 female mice were mated either to a control male mouse or to one that had been exposed at 7, 21 or 35 days previously, for 24 h to an ambient temperature of 36 ± 0.3 °C and 66 ± 5.6% relative humidity. Embryos were collected from the oviducts of mice at 14-16 h, 34-39 h or 61-65 h after mating or from the uterus at 85-90 h after mating and their developmental status was evaluated morphologically. The number of cells within blastocysts was also determined using bisbenzimide-propidium iodide staining. Paternal heat stress 7 days before mating reduced the proportion of embryos developing from 4-cell (4-C) to morulae (M), hatched blastocysts, total blastocysts and the number of inner cell mass (ICM) and trophectoderm (TE) cells in the blastocyst. Paternal heat stress 21 days prior to mating reduced the proportion of 2-C and 4-C to M embryos with no embryos developing to blastocysts. There were also increases in the number of 1-C and abnormal embryos recorded at this time. Paternal heat stress 35 days before mating decreased the proportion of 2-C embryos, expanded blastocysts and ICM and TE cells in the blastocyst. These results support previous work demonstrating that both the sperm in the epididymis and germ cells in the testis are susceptible to damage by environmental heat stress, with spermatocytes being the most vulnerable. This study also demonstrates that subtle effects on the male such as a short exposure to elevated environmental temperatures can translate to quite profound paternal impacts on early embryo development.paternal heat stress / in vivo development / mouse preimplantation embryos

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Effects of paternal heat stress on the in vivo development of preimplantation embryos in the mouse

Zhu

Setchell

2004

Reprod. Nutr. Dev.

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“…8,3 days (Clermont, 1972) previous to the count, to which the sperm transit time to the cauda of the epididymis must be added (about 5 days) (Dadoune & Alfonsi, 1984). Therefore, changes in sperm output will be recorded in cauda by 13,3 days.…”

Section: Discussionmentioning

confidence: 99%

Effects of Chronic Simulated Hypobaric Hypoxia on Mouse Spermatogenesis

et al. 2006

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SUMMARY:Reduction of O2 delivery to tissues damage them, including the seminiferous epithelium. Recently, population working in high altitude has increased, so that the study of hypobaric hypoxia on spermatogenesis becomes of interest. In this study we used two groups of male, sexually mature mice Control (C) (540 meters above sea level (masl)) and chronic simulated hypobaric hypoxia (CSHH) (4,600 masl) exposed during 8, 16, 24 or 33 days. Hematocrit; reticulocytosis; testicular, epididymal and seminal vesicle weight; seminiferous epithelium height, tubular diameter, sperm count and morphology and testicular parenchyme and spermatozoa membranes lipoperoxidation were measured. Weight of testis, epididymis and seminal vesicle were reduced but they recuperate at 33 days. Tubular diameter and epithelial height are reduced, subsequently they tend to increase without returning to normal values. The count and sperm morphology fluctuate along the exposure time. Lipoperoxidation levels of spermatozoa and testicular parenchyme are reduced. Therefore, we can conclude that exposure to CSHH induce damage in the seminiferous epithelium, decrease of lipoperoxidation in spermatozoa and testicular tissue, and damages the testicular and sperm morphology.

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“…Many authors have used radiolabelled spermatozoa to show the duration of normal epididymal transport (Orgebin-Crist, 1965;Fulka, Kopecny & Koefoed-Johnson, 1971; Dadoune & Alfonsi, 1984), but the passage of labelled spermatozoa in the tracts of vasectomized animals has not been investigated. Vasectomy is a common clinical practice with few unwanted sequelae.…”

Section: Introductionmentioning

confidence: 99%

Fate of superfluous sperm products after vasectomy and in the normal male tract of the mouse

Barratt

Cohen

1986

Reproduction

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Summary. The progression of 3H-labelled spermatozoa (thymidine or arginine) was followed through the tracts of unilaterally vasectomized, bilaterally vasectomized, oligozoospermic (t6/tw5) and normal mice; the regional lymph nodes were also investigated. The same rate of sperm production and transport was found in normal and in vasectomized tracts, down to the corpus epididymidis; there was some delay in spermatozoa entering the cauda in the vasectomized tracts. In the mouse, therefore, vasectomy does not affect the rates of sperm production or transport until just before the blockage in the swollen cauda epididymidis. Radioactivity appeared in the caudal and 'paraaortic' lymph nodes as the radioactive spermatozoa passed from the corpus, showing that this is one route of disposal of spermatozoa, or of sperm products, after vasectomy.Naturally oligozoospermic and normal mice gave similar results; again the caudal, iliac and renal lymph nodes received radioactive spermatozoa/sperm products. Some loss of (by definition) superfluous spermatozoa in the normal male tract therefore occurs naturally by this route, and we suggest that vasectomy further exploits this physiological pathway. This would account for the finding that many males do not make antisperm antibodies after vasectomy, just as normal males do not, even though their lymph nodes normally receive spermatozoa/sperm products.

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Autoradiographic investigation of sperm transit through the male mouse genital tract after tritiated thymidine incorporation

Cited by 19 publications

References 11 publications

Effects of paternal heat stress on the in vivo development of preimplantation embryos in the mouse

Effects of paternal heat stress on the in vivo development of preimplantation embryos in the mouse

Effects of Chronic Simulated Hypobaric Hypoxia on Mouse Spermatogenesis

Fate of superfluous sperm products after vasectomy and in the normal male tract of the mouse

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