Vinclozolin—No transgenerational inheritance of anti-androgenic effects after maternal exposure during organogenesis via the intraperitoneal route

Schneider, Steffen; Marxfeld, Heike; Gröters, Sibylle; Buesen, Roland; Ravenzwaay, Bennard van

doi:10.1016/j.reprotox.2012.12.003

Cited by 34 publications

(24 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Thus, early exposure of animal and humans to these widely prevalent chemicals may lead to insidious behavioral effects. Moreover, there is ample evidence in animal models that EDCs (and humans in the case of DES) can induce transgenerational effects (Newbold et al, 2000, 2006; Klip et al, 2002; Titus-Ernstoff et al, 2006; Wolstenholme et al, 2012, 2013; Doyle et al, 2013; Manikkam et al, 2013; Schneider et al, 2013; Zhang et al, 2014b). Therefore, these chemicals might already be exhuming a toll on the social lives of unborn generations.…”

Section: Discussionmentioning

confidence: 99%

Bisphenol A and phthalate endocrine disruption of parental and social behaviors

Rosenfeld

2015

Front. Neurosci.

View full text Add to dashboard Cite

Perinatal exposure to endocrine disrupting chemicals (EDCs) can induce promiscuous neurobehavioral disturbances. Bisphenol A and phthalates are two widely prevalent and persistent EDCs reported to lead to such effects. Parental and social behaviors are especially vulnerable to endocrine disruption, as these traits are programmed by the organizational-activational effects of testosterone and estrogen. Exposure to BPA and other EDCs disrupts normal maternal care provided by rodents and non-human primates, such as nursing, time she spends hunched over and in the nest, and grooming her pups. Paternal care may also be affected by BPA. No long-term study has linked perinatal exposure to BPA or other EDC and later parental behavioral deficits in humans. The fact that the same brain regions and neural hormone substrates govern parental behaviors in animal models and humans suggests that this suite of behaviors may also be vulnerable in the latter. Social behaviors, such as communication, mate choice, pair bonding, social inquisitiveness and recognition, play behavior, social grooming, copulation, and aggression, are compromised in animal models exposed to BPA, phthalates, and other EDCs. Early contact to these chemicals is also correlated with maladaptive social behaviors in children. These behavioral disturbances may originate by altering the fetal or adult gonadal production of testosterone or estrogen, expression of ESR1, ESR2, and AR in the brain regions governing these behaviors, neuropeptide/protein hormone (oxytocin, vasopressin, and prolactin) and their cognate neural receptors, and/or through epimutations. Robust evidence exists for all of these EDC-induced changes. Concern also exists for transgenerational persistence of such neurobehavioral disruptions. In sum, evidence for social and parental deficits induced by BPA, phthalates, and related chemicals is strongly mounting, and such effects may ultimately compromise the overall social fitness of populations to come.

show abstract

Section: Discussionmentioning

confidence: 99%

Bisphenol A and phthalate endocrine disruption of parental and social behaviors

Rosenfeld

2015

Front. Neurosci.

View full text Add to dashboard Cite

show abstract

“…In contrast, a different group exposed outbred female (F0) Wistar rats to vinclozolin during gestation (E6 to E15) and reported no adverse transgenerational anti-androgenic effects in F1–F4 male offspring for two separate studies (Schneider et al, 2008, 2013). The first study reported decreased and the second reported increased spermatogenic cell apoptosis in F1–F3 male offspring after maternal F0 vinclozolin treatment.…”

Section: Transgenerational Phenotypes In Mammalsmentioning

confidence: 99%

“…A study by an additional independent research group, using inbred Sprague–Dawley rats, reported no effects on spermatogenesis in F1 or F2 males after maternal (F0) exposure to vinclozolin (Inawaka et al, 2009). The reason is undetermined, but the discrepancy suggests the possible influence of genetic variations among strains (Heard and Martienssen, 2014; Inawaka et al, 2009; Schneider et al, 2013). Additionally, the original research group (Anway et al) reported intraspecies differences in susceptibility to vinclozolin in mouse strains after F0 female exposure during gestation (E7 to E13).…”

Section: Transgenerational Phenotypes In Mammalsmentioning

confidence: 99%

Elusive inheritance: Transgenerational effects and epigenetic inheritance in human environmental disease

Martos

Tang

Wang

2015

Progress in Biophysics and Molecular Biology

View full text Add to dashboard Cite

Epigenetic mechanisms involving DNA methylation, histone modification, histone variants and nucleosome positioning, and noncoding RNAs regulate cell-, tissue-, and developmental stage-specific gene expression by influencing chromatin structure and modulating interactions between proteins and DNA. Epigenetic marks are mitotically inherited in somatic cells and may be altered in response to internal and external stimuli. The idea that environment-induced epigenetic changes in mammals could be inherited through the germline, independent of genetic mechanisms, has stimulated much debate. Many experimental models have been designed to interrogate the possibility of transgenerational epigenetic inheritance and provide insight into how environmental exposures influence phenotypes over multiple generations in the absence of any apparent genetic mutation. Unexpected molecular evidence has forced us to reevaluate not only our understanding of the plasticity and heritability of epigenetic factors, but of the stability of the genome as well. Recent reviews have described the difference between transgenerational and intergenerational effects; the two major epigenetic reprogramming events in the mammalian lifecycle; these two events making transgenerational epigenetic inheritance of environment-induced perturbations rare, if at all possible, in mammals; and mechanisms of transgenerational epigenetic inheritance in non-mammalian eukaryotic organisms. This paper briefly introduces these topics and mainly focuses on (1) transgenerational phenotypes and epigenetic effects in mammals, (2) environment-induced intergenerational epigenetic effects, and (3) the inherent difficulties in establishing a role for epigenetic inheritance in human environmental disease.

show abstract

“…Interestingly, spinal agenesis and limb polymelia were shown only in F 2 generation mice of the low-dose flutamide exposure group, indicating the profile of biological disruption may be exposure concentration based and generation specific (Anway et al 2008). However, it should be noted that others have not observed such transgenerational effects of these specific compounds (Schneider et al 2013). Despite relatively high exposure concentrations, such research is likely to inform mechanisms by which human PPCP and other EC mediated biological disruption could occur.…”

Section: Numerous Examples Of Multi and Transgenerational Epigenetic mentioning

confidence: 99%

Ecotoxic pharmaceuticals, personal care products, and other emerging contaminants: A review of environmental, receptor-mediated, developmental, and epigenetic toxicity with discussion of proposed toxicity to humans

Wilkinson

Hooda

Barker

et al. 2015

Critical Reviews in Environmental Science and Technology

171

View full text Add to dashboard Cite

Vinclozolin—No transgenerational inheritance of anti-androgenic effects after maternal exposure during organogenesis via the intraperitoneal route

Cited by 34 publications

References 44 publications

Bisphenol A and phthalate endocrine disruption of parental and social behaviors

Bisphenol A and phthalate endocrine disruption of parental and social behaviors

Elusive inheritance: Transgenerational effects and epigenetic inheritance in human environmental disease

Ecotoxic pharmaceuticals, personal care products, and other emerging contaminants: A review of environmental, receptor-mediated, developmental, and epigenetic toxicity with discussion of proposed toxicity to humans

Contact Info

Product

Resources

About