Hormonal Antagonism to the Antispermatogenic Effect of Ethylenedimethanesulphonate in Rats

Jackson, H.; Cm, Jackson; Jones, Philip R.

doi:10.1530/jrf.0.0340133

Cited by 18 publications

(8 citation statements)

References 8 publications

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“…Many of the cytological changes that occur within the seminiferous tubules after EDS have been described by Cooper & Jackson (1970) and, more recently, by Bartlett et al (1986). Within 6 days of EDS administration, mature spermatids at stages VII-VIII of the spermatogenic cycle disappear from the testis (Cooper & Jackson, 1970) and maximum disruption of spermatogenesis occurs in weeks 2-4 , corresponding to a period of infertility as reported by Jackson, Jackson & Jones (1973). Spermatogenesis and fertility were restored by day 45 (Cooper & Jackson, 1970).…”

Section: Introductionmentioning

confidence: 96%

Effects of ethane dimethane sulphonate (EDS) on seminiferous tubule function in rats

et al. 1987

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The effects of a single injection of ethane dimethane sulphonate (EDS) on aspects of seminiferous tubule function were assessed over a period of 49 days. Ethane dimethane sulphonate, which is known to cause destruction of Leydig cells, reduced the levels of testosterone in both serum and testicular interstitial fluid for 21 days, after which recovery occurred. The low testosterone levels were associated with elevated serum levels of LH and FSH. Daily sperm production was decreased from 14 to 42 days post-EDS but returned to control levels at 49 days. The production of seminiferous tubule fluid, measured after unilateral efferent duct ligation, decreased significantly at 7 and 14 days but then recovered. The testicular content of androgen binding protein (ABP) was decreased from 14 to 28 days but returned to normal thereafter. These results demonstrate significant effects on seminiferous tubule function, which may be due to the decrease in testosterone or be associated with a direct effect of EDS.

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Section: Introductionmentioning

confidence: 96%

Effects of ethane dimethane sulphonate (EDS) on seminiferous tubule function in rats

et al. 1987

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“…These changes have been correlated with impaired testicular androgen biosynthetic capacity (Bu'Lock & Jackson, 1975; Morris & McCluckie, 1979) and elevated serum LH levels (Jackson & Morris, 1977). A 9-day course of testosterone, with the EDS given on Day 4, provided temporary protection of the spermatogenic epithelium (histologically assessed) and maintained some degree of fertility (Jackson, Jackson & Jones, 1973); subsequently the characteristic degenerative changes developed followed by a period of infertility. By contrast, 9 daily injections of hCG (100 i.u.)…”

Section: Introductionmentioning

confidence: 99%

Comparative protective actions of gonadotrophins and testosterone against the antispermatogenic action of ethane dimethanesulphonate

Cm¹,

Jackson²

1984

Reproduction

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“…However, this activity is not related to alky¬ lation of the spermatogenic cells and it is now well established that the Leydig cell is the primary target. Fertility after EDS can be maintained by human chorionic gonadotrophin (hCG) or testosterone (Jackson, Jackson & Jones, 1973). The weights of the seminal vesicles and the ventral prostate, and the serum testosterone and luteinizing hormone (LH) con¬ centrations in EDS-treated rats are similar to those of castrated rats.…”

Section: Introductionmentioning

confidence: 99%

“…In addition, testicular hCG binding was investigated. Human chorionic gonadotrophin protects the testis from EDS which suggests that the LH-receptor complex on the Leydig cell membrane may be involved in the cytotoxic activity (Jackson et al 1973;Jackson ¿¿Jackson, 1984). A description of the Leydig cell LH-receptor binding during EDS treatment may help to elucidate how EDS specifically destroys Leydig cells.…”

Section: Introductionmentioning

confidence: 99%

Leydig cell resistance to the cytotoxic effect of ethylene dimethanesulphonate in the adult rat testis

Morris¹

1985

Journal of Endocrinology

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Weekly doses of the Leydig cell cytotoxic ethylene dimethanesulphonate (EDS) were administered to adult male rats in an attempt to study the endocrine activity of the testis in the absence of Leydig cells. One week after the first dose serum testosterone and LH concentrations and seminal vesicle weights were close to levels in castrated rats and testicular human chorionic gonadotrophin (hCG) binding was severely depressed. These changes were maintained for a further week but subsequently began to return to, but did not achieve, control levels. After six weekly doses seminal vesicle weight and serum testosterone concentrations were significantly higher than in the castrated rats. Serum LH concentrations were declining towards control values at 4 weeks but had risen again at 6 weeks. Serum FSH concentrations were raised to about 50% of the value in castrated rats throughout the period studied. Testis weight and hCG binding, which initially fell, were partially restored at 6 weeks and spermatogenesis was recovering. The data show that responses of the testis to multiple doses of EDS are similar to those after a single dose. This apparent resistance indicates that the regenerating Leydig cells are functionally different from the mature Leydig cell. The similarities between the maturing Leydig cell seen after EDS destruction and those in the immature rat suggest that EDS will provide a valuable model for the investigation of Leydig cell physiology.

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Hormonal Antagonism to the Antispermatogenic Effect of Ethylenedimethanesulphonate in Rats

Cited by 18 publications

References 8 publications

Effects of ethane dimethane sulphonate (EDS) on seminiferous tubule function in rats

Effects of ethane dimethane sulphonate (EDS) on seminiferous tubule function in rats

Comparative protective actions of gonadotrophins and testosterone against the antispermatogenic action of ethane dimethanesulphonate

Leydig cell resistance to the cytotoxic effect of ethylene dimethanesulphonate in the adult rat testis

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