Late-gestation exogenous oestrogen inhibits testicular descent in fetal mice despite M�llerian duct regression

Luthra, Meera; Hutson, John M.

doi:10.1007/bf00177495

Cited by 11 publications

(5 citation statements)

References 13 publications

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“…The interference by MBP on testicular descent was greatest when administered to pregnant rats during the critical period of transabdominal migration of the testis. These findings are similar to those in prenatally oestrogen‐treated mice, in which oestrogen inhibited both the transabdominal migration of the testis and the regression of the Müllerian duct during the first phase of testicular descent [11,20]. Grasso et al [21] suggested that some phthalate esters reduce the degree of FSH binding to Sertoli cells, which secrete MIS.…”

Section: Discussionsupporting

confidence: 77%

Time‐specific effects of mono‐n‐butyl phthalate on the transabdominal descent of the testis in rat fetuses

et al. 2000

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Objective To determine the time-speci®c effects of monon-butyl phthalate (MBP) on the transabdominal migration of the testis in fetal rats. Materials and methods Three groups of pregnant rats were administered MBP by stomach-tube feeding when the fetus was at 7±10 days of gestation in group 1, 11±14 days in group 2, and 15±18 days in group 3; controls (group 4) were given vehicle only from 7±18 days. At 20 days of gestation the fetuses were obtained by Caesarean section, and the position of the testes, the development of the gubernaculum, cranial suspensory ligament and the epididymis were examined. Results The timed intervals of MBP administration showed that the maximum inhibition of transabdominal testicular descent was at 15±18 days of gestation.There was an elongated gubernaculum and hypertrophic cranial suspensory ligament in the MBPtreated rat fetuses. Furthermore, the epididymis showed a few small ducti deferentia, although there were no remarkable changes in either the Sertoli and Leydig cells in these testes. The mean (SEM) content of testicular testosterone was signi®cantly less (P<0.001) in the MBP-treated rats, at 50.9 (3.8) pg/ testis, than in the controls, at 676 (33.3) pg/testis. Conclusions These ®ndings indicate that a brief exposure to MBP during fetal development can inhibit the transabdominal migration of the testis and reduce testosterone content in rats, although the relationship between migration and the testicular testosterone content remains unknown.

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Section: Discussionsupporting

confidence: 77%

Time‐specific effects of mono‐n‐butyl phthalate on the transabdominal descent of the testis in rat fetuses

et al. 2000

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“…It has been proposed that testicular descenr occurs in two steps which are separated in time and are under separate hormonal control (Backhouse & Butler, 1960;Habenicht & Neumann, 1983, Hutson, 1985. Transabdominal testicular descent occurs between weeks 10 and 14-15 of gestation in the human (Jirasek, 1971) and between days 15 and 17 of gestation in the mouse (Hadziselimovic et al, 1980;Hadziselimovic, 1983) under the putative control of MIS (Luthra & Hutson, 1990). The inguino-scrota1 phase of testicular descent occurs after week 26 of gestation in humans (Heyns, 1987) and around birth in mice (Hadziselimovic, 1980).…”

Section: Discussionmentioning

confidence: 99%

“…(4) Oestrogen may cause the retention of the Miillerian duct by suppressing MIS action, and the Mullerian duct mechanically hinders descent of the testis . (5) Oestrogen may act as an anti-MIS and cause both inhibited gubernacular development and cryptorchidism as well as retention of the Mullerian ducts (Luthra & Hutson, 1990).…”

Section: Discussionmentioning

confidence: 99%

“…Mullerianinhibiting substance (MIS), which is secreted h-om the fetal testis, has been proposed to cause the distal gubernacular enlargement or 'swelling' as well as regression of the Miillerian duct . Exposure to oestrogens during gestation prevents both Miillerian duct regression and transabdominal testicular descent in male mice (Raynaud & Raynaud, 1958;McLachlan et al, 1975;Habenicht & Neumann, 1983;Luthra & Hutson, 1990), possibly by the suppression of MIS action . However, it is reported that fetal rats exposed to androgen-blockade with flutamide during the phase of transabdominal testicular descent often show cryptorchidism postnatally (Spencer et a/., 1991;Husmann & McPhaul, 1991;Goh et al, 1994;Husinann et al, 1994;Shono et al, 1994a), and the cause of this is suspected to be flutamide-induced inhibition of gubernacular development (Spencer et al, 1991;Shono et al 1994a).…”

Section: Introductionmentioning

confidence: 99%

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Scanning electron microscopy shows inhibited gubernacular development in relation to undescended testes in oestrogen‐treated mice

Shono¹,

Hutson²,

Watts³

et al. 1996

Int J of Andrology

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The morphological relationship between transabdominal testicular descent and the 'swelling reaction' of the gubernaculum was investigated in oestrogen-treated fetal mice by using scanning electron microscopy (scanning EM). In addition, flutamide was also administered to pregnant mice to determine whether androgens cause gubernacular growth and transabdominal testicular descent in offspring. In oestrogen-treated fetal mice, scanning EM showed that both the gubernacular 'swelling reaction' and transabdominal testicular descent were inhibited, in addition to inhibition of Müllerian duct regression. The gubernaculum showed a flat, thin bulb (widest diameter 0.25 +/- 0.04 mm) and an elongated cord (1.28 +/- 0.41 mm) after oestrogen treatment in utero, which was significantly different in appearance from that in normal control mice (width 0.44 mm +/- 0.06 mm, p < 0.001; length 0.27 +/- 0.19 mm, p < 0.0001). However, flutamide-treated mice showed much more normal gubernacular enlargement and transabdominal testicular descent. The width of the gubernacular bulb after flutamide exposure was 0.44 +/- 0.05 mm, which was comparable to that in control animals; the length of the intra-abdominal gubernaculum (0.44 +/- 0.15 mm) was slightly longer than in controls (p < 0.02). These results suggest that both the swelling reaction of the gubernaculum and transabdominal testicular migration are blocked by prenatal exposure to oestrogen. However, oestrogen exposure of the fetus does not block the swelling reaction of the gubernaculum by acting as an antiandrogen.

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“…There is a wealth of data showing that male animals exposed in utero or perinatally to exogenous oestrogens (diethylstilboestrol, ethinyl oestradiol, bisphenol A) and anti-androgens [flutamide, vinclozolin, 1,1-dichloro-2,2-bis(p-chlorophenyl) ethylene (DDE), 1,1,1-trichloro-2,2-bis(4-chlorophenyl)ethane (DDT)] develop hypospadias, undescended testis, low sperm counts or, in the worst case, intersex conditions, teratomas and Leydig cell tumours (Viguier-Martinez et al, 1983;Newbold and McLachlan, 1985;Yasuda et al, 1985;Luthra and Hutson, 1989;Walker et al, 1990;Kelce et al, 1997). A recent report provided experimental evidence that ubiquitous phthalates, can also hamper testicular descent in rats when administered prenatally (Shono et at., 2000).…”

Section: Evidence From Animal Studies and Wildlifementioning

confidence: 99%

Testicular dysgenesis syndrome: an increasingly common developmental disorder with environmental aspects

Meyts

Main

2001

APMIS

679

906

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Numerous reports have recently focused on various aspects of adverse trends in male reproductive health, such as the rising incidence of testicular cancer; low and probably declining semen quality; high and possibly increasing frequencies of undescended testis and hypospadias; and an apparently growing demand for assisted reproduction. Due to specialization in medicine and different ages at presentation of symptoms, reproductive problems used to be analysed separately by various professional groups, e.g. paediatric endocrinologists, urologists, andrologists and oncologists. This article summarizes existing evidence supporting a new concept that poor semen quality, testis cancer, undescended testis and hypospadias are symptoms of one underlying entity, the testicular dysgenesis syndrome (TDS), which may be increasingly common due to adverse environmental influences. Experimental and epidemiological studies suggest that TDS is a result of disruption of embryonal programming and gonadal development during fetal life. Therefore, we recommend that future epidemiological studies on trends in male reproductive health should not focus on one symptom only, but be more comprehensive and take all aspects of TDS into account. Otherwise, important biological information may be lost.

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Late-gestation exogenous oestrogen inhibits testicular descent in fetal mice despite M�llerian duct regression

Cited by 11 publications

References 13 publications

Time‐specific effects of mono‐n‐butyl phthalate on the transabdominal descent of the testis in rat fetuses

Time‐specific effects of mono‐n‐butyl phthalate on the transabdominal descent of the testis in rat fetuses

Scanning electron microscopy shows inhibited gubernacular development in relation to undescended testes in oestrogen‐treated mice

Testicular dysgenesis syndrome: an increasingly common developmental disorder with environmental aspects

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