Effect of low dose of vinclozolin on reproductive tract development and sperm parameters in CD1 outbred mice

Elzeinova, Fatima; Nováková, V.; Buckiová, Daniela; Kubátová, Alena; Pěknicová, Jana

doi:10.1016/j.reprotox.2008.09.007

Cited by 39 publications

(22 citation statements)

References 36 publications

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“…This includes chemicals that occur naturally in plants such as genistein and resveratrol (phytoestrogens) and also man-made chemicals such as bisphenol-A, diethylstilbestrol and vinclozolin (xenoestrogens), which can disrupt the endocrine function of animals and negatively influence spermatogenesis and sperm parameters (Peknicová et al 2002, Kyselova et al 2003, 2004, Elzeinova et al 2008. These chemicals again mainly act by binding to estrogen receptors (Kuiper et al 1998, Sohoni & Sumpter 1998, Akingbemi & Hardy 2001 and trigger a rapid non-genomic signaling response.…”

Section: Introductionmentioning

confidence: 99%

In vivo exposure to 17β-estradiol triggers premature sperm capacitation in cauda epididymis

Děd¹,

Šebková²,

Černá³

et al. 2013

Reproduction

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Estrogens play a crucial role in spermatogenesis and estrogen receptor a knock-out male mice are infertile. It has been demonstrated that estrogens significantly increase the speed of capacitation in vitro; however this may lead to the reduction of reproductive potential due to the decreased ability of these sperm to undergo the acrosome reaction. To date the in vivo effect of estrogens on the ability of sperm to capacitate has not been investigated. Therefore, in this study, we exposed mice (nZ24) to 17b-estradiol (E 2 ) at the concentration of 20 ng/ml either during puberty from the fourth to seventh week of age (nZ8), or continuously from birth for a period of 12 weeks (nZ8) at which age the animals from both groups were killed. The capacitation status of epididymal and testicular sperm was analysed by tyrosine phosphorylation (TyrP) antibody (immunofluorescence and western blot) and chlortetracycline (CTC) assay. According to our results, in vivo exposure to increased E 2 concentrations caused premature sperm capacitation in the epididymis. The effect of E 2 , however, seems reversible because after the termination of the exposure premature epididymal sperm capacitation is decreased in animals treated during puberty. Furthermore the changes in epididymal sperm capacitation status detected by TyrP and CTC positively correlate with plasma levels of E 2 and the expression of the estrogen-dependent trefoil factor 1 (Tff1) gene in testicular tissue. Therefore, our data implicate that in vivo exposure to E 2 under specific conditions leads to the premature capacitation of mouse sperm in epididymis with a potential negative impact on the sperm reproductive fitness in the female reproductive tract.

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Section: Introductionmentioning

confidence: 99%

In vivo exposure to 17β-estradiol triggers premature sperm capacitation in cauda epididymis

Děd¹,

Šebková²,

Černá³

et al. 2013

Reproduction

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“…These effects are paralleled by a decrease in the sperm concentration observed only in F1. Therefore, it proposes a mechanism for the previously observed effects of VCZ on the rodent reproductive system (Shimamura et al 2002, Anway et al 2005, Buckley et al 2006, Elzeinova et al 2008. By analogy, we can postulate that the reported effects of EDCs on human male spermatogenesis and fertility rates (Roeleveld & Bretveld 2008) might involve imprinting alterations in the sperm.…”

Section: Peg3mentioning

confidence: 90%

“…It also induced decreases in the anogenital distance and in the prostate weight (Buckley et al 2006, Elzeinova et al 2008. Eventually, VCZ affected spermatogenesis inducing decreases in sperm number and motility, sperm head abnormalities, and apoptosis in the seminiferous tubules germ cells (Shimamura et al 2002, Anway et al 2005, Buckley et al 2006, Elzeinova et al 2008). An intriguing feature of VCZ is that the effects on male genital tract and spermatogenesis were found to be transgenerational, extending from F1 to F4 (Anway et al 2005(Anway et al , 2006(Anway et al , 2008.…”

Section: Introductionmentioning

confidence: 98%

“…It masculinized females (longer urethras), feminized males (hypospadias), and increased the expression of progesterone receptors in both genders (Buckley et al 2006). It also induced decreases in the anogenital distance and in the prostate weight (Buckley et al 2006, Elzeinova et al 2008. Eventually, VCZ affected spermatogenesis inducing decreases in sperm number and motility, sperm head abnormalities, and apoptosis in the seminiferous tubules germ cells (Shimamura et al 2002, Anway et al 2005, Buckley et al 2006, Elzeinova et al 2008).…”

Section: Introductionmentioning

confidence: 99%

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Transgenerational effects of the endocrine disruptor vinclozolin on the methylation pattern of imprinted genes in the mouse sperm

Stouder¹,

2010

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Endocrine-disrupting chemicals (EDCs), among which is the antiandrogen vinclozolin (VCZ), have been reported to affect the male reproductive system. In this study, VCZ was administered to pregnant mice at the time of embryo sex determination, and its possible effects on the differentially methylated domains (DMDs) of two paternally (H19 and Gtl2) and three maternally (Peg1, Snrpn, and Peg3) imprinted genes were tested in the male offspring. The CpGs methylation status within the five gene DMDs was analyzed in the sperm, tail, liver, and skeletal muscle DNAs by pyrosequencing. In the sperm of controls, the percentages of methylated CpGs were close to the theoretical values of 100 and 0% in paternally or maternally imprinted genes respectively. VCZ decreased the percentages of methylated CpGs of H19 and Gtl2 (respective values 83.1 and 91.5%) and increased those of Peg1, Snrpn, and Peg3 (respective values 11.3, 18.3, and 11.2%). The effects of VCZ were transgenerational, but they disappeared gradually from F1 to F3. The mean sperm concentration of the VCZ-administered female offspring was only 56% of that of the controls in the F1 offspring, and it was back to normal values in the F2 and F3 offspring. In the somatic cells of controls, the percentages of methylated CpGs were close to the theoretical value of 50% and, surprisingly, VCZ altered the methylation of Peg3. We propose that the deleterious effects of VCZ on the male reproductive system are mediated by imprinting defects in the sperm. The reported effects of EDCs on human male spermatogenesis might be mediated by analogous imprinting alterations.

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“…Vinclozolin (VCZ), a fungicide possessing an anti-androgenic activity affected spermatogenesis inducing decreases in sperm number and motility and an increase in apoptosis in the seminiferous tubules germ cells (Shimamura et al 2002, Anway et al 2005, Buckley et al 2006, Elzeinova et al 2008. MXC, administered perinatally or during gestation, was also found to affect spermatogenesis in the adult or in the offspring respectively (Chapin et al 1997, Anway et al 2005).…”

Section: Introductionmentioning

confidence: 99%

Specific transgenerational imprinting effects of the endocrine disruptor methoxychlor on male gametes

2011

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Endocrine-disrupting chemicals (EDCs), among which methoxychlor (MXC), have been reported to affect the male reproductive system. This study evaluates the possible deleterious effects of MXC on imprinted genes. After administration of the chemical in adult male mice or in pregnant mice we analyzed by pyrosequencing possible methylation defects in two paternally imprinted (H19 and Meg3 (Gtl2)) and three maternally imprinted (Mest (Peg1), Snrpn, and Peg3) genes in the sperm and in the tail, liver, and skeletal muscle DNAs of the adult male mice and of the male offspring. MXC treatment of adult mice decreased the percentages of methylated CpGs of Meg3 and increased those of Mest, Snrpn, and Peg3 in the sperm DNA. MXC treatment of pregnant mice decreased the mean sperm concentrations by 30% and altered the methylation pattern of all the imprinted genes tested in the F1 offspring. In the latter case, MXC effects were transgenerational but disappeared gradually from F1 to F3. MXC did not affect imprinting in the somatic cells, suggesting that it exerts its damaging effects via the process of reprogramming that is unique to gamete development. A systematic analysis at the CpG level showed a heterogeneity in the CpG sensitivity to MXC. This observation suggests that not only DNA methylation but also other epigenetic modifications can explain the transgenerational effects of MXC. The reported effects of EDCs on human male spermatogenesis might be mediated by complex imprinting alterations analogous to those described in this study.

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Effect of low dose of vinclozolin on reproductive tract development and sperm parameters in CD1 outbred mice

Cited by 39 publications

References 36 publications

In vivo exposure to 17β-estradiol triggers premature sperm capacitation in cauda epididymis

In vivo exposure to 17β-estradiol triggers premature sperm capacitation in cauda epididymis

Transgenerational effects of the endocrine disruptor vinclozolin on the methylation pattern of imprinted genes in the mouse sperm

Specific transgenerational imprinting effects of the endocrine disruptor methoxychlor on male gametes

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