Neonatal exposure of male rats to estradiol benzoate causes rete testis dilation and backflow impairment of spermatogenesis

Aceitero, J; Llanero, Marcos; Parrado, Rafael; Peña, Esteban Gilberto Ramos; López-Beltrán, Antonio

doi:10.1002/(sici)1097-0185(199809)252:1<17::aid-ar3>3.0.co;2-b

Cited by 47 publications

(11 citation statements)

References 44 publications

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“…The increased levels of LH together with decreased levels of serum testosterone are indicative of decreased steroidogenic ability of the testes of the mice transplacentally exposed to progesterone. Earlier reports also indicate that neonatal exposure of male rats to DES resulted in suppression of androgen action and also abnormalities of the male reproductive tract (Arai et al 1983, Newbold & McLachlan 1985, Marselos & Tomatis 1992, Aceitero et al 1998, Fisher et al 1998, Khan et al 1998, Sharpe et al 1998, McKinnell et al 2001.…”

Section: Discussionmentioning

confidence: 96%

Recovery of suppressed male reproduction in mice exposed to progesterone during embryonic development by testosterone

Harini¹,

Sainath²,

Reddy³

2009

Reproduction

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The present study aimed to examine whether transplacental exposure to progesterone caused male reproductive abnormalities and whether the changes can be reversed after testosterone administration. Progesterone was injected to mice on day 1, 3, and 7 of pregnancy. The male pups (F1 generation) were allowed to grow for 50 days and assessed for reproductive performance. Gestational exposure to progesterone (7 mg/kg body weight) resulted in significant body weight gain with a decrease in reproductive tissue indices in mice. Total sperm count, viable sperm, and motile sperm decreased in experimental mice. Hypo-osmotic swelling test revealed that experimental mice sperm membrane integrity was severely altered. The activity levels of testicular steroidogenic marker enzymes (hydroxy-delta-5-steroid dehydrogenase, 3 beta-and steroid delta-isomerase cluster (HSD3B) and hydroxysteroid (17-beta) dehydrogenase 1 (HSD17B)) decreased significantly in mice exposed to progesterone during embryonic development when compared with the controls. The levels of serum testosterone decreased with an increase in serum FSH and LH in mice exposed to progesterone during embryonic development. Prenatal exposure to progesterone caused significant reduction in the number of spermatozoa and increase in the lumen of seminiferous tubule. The experimental mice that cohabited with normal females showed fertility reduction. Administration of testosterone (4.16 mg/kg body weight) on postnatal day 20, 30, and 40 to progesterone-exposed prenates resulted in recovery of progesterone-induced suppressed male reproduction. It is suggested that the impairment of male reproduction in mice exposed to progesterone during embryonic development could be mediated through the inhibition of testosterone production. These results also indicate that in utero exposure to progesterone affects male reproduction and that supplementation of testosterone restores the suppressed male reproduction.

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Section: Discussionmentioning

confidence: 96%

Recovery of suppressed male reproduction in mice exposed to progesterone during embryonic development by testosterone

Harini¹,

Sainath²,

Reddy³

2009

Reproduction

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“…It has been reported that several synthetic and natural chemicals through either maternal or neonatal exposure induced developmental disorder of the male and female offspring in rats [1,9,15,24,25,41]. However, the effect on the male and female reproductive organs of the offspring maternally exposed to BP was not yet reported and poorly understood.…”

Section: Discussionmentioning

confidence: 99%

Decreased Sperm Number and Motile Activity on the F1 Offspring Maternally Exposed to Butyl p-Hydroxybenzoic Acid(Butyl Paraben).

et al. 2002

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ABSTRACT. Butyl p-hydroxybenzoic acid (butyl paraben, BP) is widely used as a preservative in food and cosmetic products. Routledge et al showed that BP is weakly estrogenic in both in vitro and in vivo (rat uterotrophic) analyses. We investigated whether maternal exposures to BP during gestation and lactation periods affected the development of the reproductive organs of the F1 offspring. Pregnant Sprague-Dawley rats were injected subcutaneously with 100 or 200 mg/kg of BP from gestation day (GD) 6 to postnatal day (PND) 20. In the group exposed to 200 mg/kg of BP, the proportion of pups born alive and the proportion of pups surviving to weaning were decreased. The body weights of female offspring were significantly decreased at PND 49. The weights of testes, seminal vesicles and prostate glands were significantly decreased in rats exposed to 100 mg/kg of BP on PND 49. In contrast, the weights of female reproductive organs were not affected by BP. The sperm count and the sperm motile activity in the epididymis were significantly decreased at doses of 100 and 200 mg/kg of BP. In accordance with the sperm count in the epididymis, the number of round spermatids and elongated spermatids in the seminiferous tubule (stage VII) were significantly decreased by BP. Testicular expression of estrogen receptor (ER)-α and ER-β mRNA was significantly increased in 200 mg/kg of BP treated group at PND 90. Taken together, these results indicated that maternal exposure of BP might have adverse effects on the F1 male offspring.KEY WORDS: butyl p-hydroxybenzoic acid, male reproductive organ, maternal exposure, sperm.

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“…Administration or deprivation of oestrogen, both during development and in the adult, has been shown to cause structural and functional changes in the male reproductive tract, including infertility. Neonatal treatment of male rats with oestrogenic chemicals reduces testicular and epididymal sperm concentration, plasma testosterone (Goyal et al 2003, Sharpe et al 2003, Sertoli cell number (Atanassova et al 2005), alters testicular gene expression (Adachi et al 2004) and causes rete tubule distension and reduced epithelial height in the efferent ducts (Aceitero et al 1998, Fisher et al 1998, 1999. The absence of a functional ER also causes distension of the rete testes, efferent ducts and epididymides, and causes infertility (Lubahn et al 1993, Eddy et al 1996, Hess et al 2000.…”

Section: Introductionmentioning

confidence: 99%

Acute exposure of adult male rats to dietary phytoestrogens reduces fecundity and alters epididymal steroid hormone receptor expression

Glover¹,

Assinder²

2006

Journal of Endocrinology

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Phytoestrogens are plant-derived compounds with oestrogenic activity. They are common in both human and animal diets, particularly through soy-based foods. This study assessed whether exposure of adult male rats to a high phytoestrogen diet for 3-25 days affected their fertility, and assessed possible mechanisms through which phytoestrogens may disrupt fertility. Adult males, fed a high phytoestrogen diet for 3 days, demonstrated significantly reduced fecundity. This effect was transient, with fecundity returning to control levels by day 12. The expression of oestrogen receptor-and androgen receptor mRNA was increased in the initial segment of the epididymis, but decreased in the cauda epididymis following 3 days on the high phytoestrogen diet. Epididymal sperm counts cannot account for the reduction in fertility at day 3. However, lipid peroxidation of epididymal sperm was significantly increased in animals fed a high phytoestrogen diet for 3 days. Disruption of the steroid regulation of the epididymis by phytoestrogens may alter its function, resulting in decreased quality of sperm, and thereby reducing fecundity.

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Neonatal exposure of male rats to estradiol benzoate causes rete testis dilation and backflow impairment of spermatogenesis

Cited by 47 publications

References 44 publications

Recovery of suppressed male reproduction in mice exposed to progesterone during embryonic development by testosterone

Recovery of suppressed male reproduction in mice exposed to progesterone during embryonic development by testosterone

Decreased Sperm Number and Motile Activity on the F1 Offspring Maternally Exposed to Butyl p-Hydroxybenzoic Acid(Butyl Paraben).

Acute exposure of adult male rats to dietary phytoestrogens reduces fecundity and alters epididymal steroid hormone receptor expression

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