Enhancement of sperm transport through the rat epididymis after castration

Sujarit, S.; Pholpramool, Chumpol

doi:10.1530/jrf.0.0740497

Cited by 36 publications

(20 citation statements)

References 16 publications

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“…There was a one-week lag in the chronological peak in the frequency of morphologically abnormal spermatozoa between caput and cauda epididymis. This phenomenon seems in agreement with the report of Sujarit and Pholpramool (1985), in which they have indicated 8 days for the transportation of spermatozoa from caput to cauda epididymis. In this sense, decreased morphologically abnormal spermatozoa in caput epididymis in Week 4 suggests the likelihood of recovery in the frequency of morphologically abnormal spermatozoa in cauda epididymis in Week 5 and later.…”

Section: Discussionsupporting

confidence: 93%

“…In this figure, total transit time of spermatozoa from the initial caput segment to vas deferens was set at 11 days. Breakdown of the time is as follows: 8 days for the transit of epididymal spermatozoa from the initial caput segment to the caudal epididymis in rats (Sujarit and Pholpramool, 1985), and 3 days for caudal spermatozoa to move into the vas deferens (adopted from the data in mice, Sega and Owens, 1978).…”

Section: Discussionmentioning

confidence: 99%

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A Time-Course Characterization of Male Reproductive Toxicity in Rats Treated With Methyl Methanesulphonate (Mms)

et al. 2005

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-Methyl methanesulphonate (MMS), a potent alkylating agent and testicular toxicant, was orally administered to rats for 5 days at doses of 20, 30, and 40 mg/kg. During the recovery period of 5 weeks, males were evaluated for multiple endpoints such as organ weights, fertility, and sperm parameters. The 5-week recovery periods are designated as follows: Day 1 (1 day after final treatment); Week 1, Week 2, Week 3, Week 4, and Week 5 (first, second, third, fourth, and fifth week after final treatment). A clear time-course of dominant lethals was observed. The peak severities of the dominant lethals were observed in Week 2. It was judged that the most sensitive cellular targets for the dominant lethals are late spermatids. Sperm examination revealed a clear time-course and dose-dependent changes in the frequency of sperm morphological abnormalities. The peak severities of the sperm morphological alterations in cauda epididymis were observed in Week 4. Sensitive cellular stages for the induction of sperm morphological abnormalities were judged to be late spermatocytes and early spermatids. The most frequently observed type of morphologically abnormal spermatozoa was tailless sperm, followed by no-hook head sperm. Although the initial cause for both sperm morphological alterations and dominant lethals was suggested to be genetic insult to the germ cells, there were no obvious relationships observed between these two findings.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

A Time-Course Characterization of Male Reproductive Toxicity in Rats Treated With Methyl Methanesulphonate (Mms)

et al. 2005

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“…In the current study, morphologically abnormal spermatozoa increased from Week 3 and the increased values lasted until Week 5. The presumable exposure periods of germ cells in these recovery periods were stages from the leptotene to mid spermatid in the current study (total transit time for spermatozoa from the initial caput segment to cauda epididymis was considered to be 8 days [12]) which was completely consistent with the UDS observed in mice. Furthermore, peak severity in the frequency of morphologically abnormal spermatozoa was observed in Week 4, in which germ cells were assumed to be exposed to MMS d urin g the pe riod of late pachy ten e spermatocytes and early spermatids.…”

Section: Discussionsupporting

confidence: 84%

Evaluation of Testicular Toxicity and Sperm Morphology in Rats Treated with Methyl Methanesulphonate (MMS)

et al. 2005

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Abstract. Methyl methanesulphonate (MMS), a potent alkylating agent and testicular toxicant, was orally administered to rats for 5 days at 40 mg/kg. During the recovery period of up to 5 weeks, males were evaluated for testicular toxicity and sperm morphology. The 5-week recovery period were designated as follows: Day 1 (the day after final treatment); Week 1, Week 2, Week 3, Week 4 and Week 5 (1, 2, 3, 4 and 5 weeks after final treatment). Morphologically abnormal sperm increased beginning in Week 3, peaked in Week 4 and declined slightly in Week 5. Histopathological examinations indicated retention of step 19 spermatids at stage IX from Day 1 through Week 3. Quantitative evaluation of spermatogenic cells indicated a decrease in the number of late pachytene spermatocytes and early spermatids on Day 1. TUNEL examination showed a significantly high frequency of apoptosis in the meiosis cells in Week 1. In the present study, genetic damage induced by treatment with MMS affected spermatogenesis and a wide variety of spermatogenic cells in the testis. Apoptosis in the course of meiosis seemed to be involved in the elimination process of genetically insulted germ cells, and this process seems to play an important role in eliminating and/or decreasing the germ cells with retention of spermatids and the potential to express morphologically abnormal spermatozoa.

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“…Although this study used a lower dose of DES compared with that in the above-cited study, we speculate that DES has the effect of retarding epididymis development. In addition, a study reported that decreased testosterone concentrations speed up the passage of sperms through the epididymis (Sujarit and Pholpramool, 1985); therefore, the epididymis weight decrease may have been influenced not only by the direct action of DES on the epididymis but also by a decrease in the amount of the sperm accumulated in the epididymides.…”

Section: Discussionmentioning

confidence: 99%

Effects of Maternal Exposure to a Low Dose of Diethylstilbestrol on Sexual Dimorphic Nucleus Volume and Male Reproductive System in Rat Offspring

Yamamoto¹,

Shirai²,

Tamura³

et al. 2005

J. Toxicol. Sci.

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-Diethylstilbestrol (DES) was administered subcutaneously at 0.5, 1.5 or 4.5 µg/kg/day (DES 0.5, 1.5 and 4.5 groups, respectively) to pregnant SD rats daily on days 7-21 of gestation, to investigate its effects on the development and functions of the reproductive system in their male offspring. Of the 10 pregnant rats in the DES 4.5 group, only 1 delivered, and this rat could not suckle the pups. Rat pups in the DES 0.5 and 1.5 groups were autopsied at 1, 3, 6 and 15 weeks after birth. The testosterone concentrations in the DES 1.5 and 0.5 groups at 6 weeks were significantly decreased and the plasma LH concentrations were not altered. In the DES 1.5 group, DES treatment did not change the volume of the sexually dimorphic nucleus in the preoptic area (SDN-POA) in the male offspring, although this dose of DES increased the volume of SDN-POA in female offspring. The DES treatment altered frequencies in the cycles of the seminiferous tubules, and suppressed histological maturation in the epididymis and the prostate weight. These observations indicate that prenatally administered DES impairs testicular endocrine function continuously as well as putuitary function, but the induced low level of testosterone disrupts spermatogensis and permanently inhibits the morphological development of epididymis and prostate.

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Enhancement of sperm transport through the rat epididymis after castration

Cited by 36 publications

References 16 publications

A Time-Course Characterization of Male Reproductive Toxicity in Rats Treated With Methyl Methanesulphonate (Mms)

A Time-Course Characterization of Male Reproductive Toxicity in Rats Treated With Methyl Methanesulphonate (Mms)

Evaluation of Testicular Toxicity and Sperm Morphology in Rats Treated with Methyl Methanesulphonate (MMS)

Effects of Maternal Exposure to a Low Dose of Diethylstilbestrol on Sexual Dimorphic Nucleus Volume and Male Reproductive System in Rat Offspring

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