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The possibility of epigenetic transmission of defects induced by teratogens

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    Conversely, overnutrition and obesity in the F0 dam can also yield phenotypes in the F2 and F3 generation (Dunn and Bale, 2009, 2011; Gniuli et al., 2008). Environmental exposure to chemical agents also leads to increased metabolic disease susceptibility in subsequent generations (Baccarelli and Bollati, 2009; Holliday, 1998; Skinner et al., 2010). Interestingly, acquired behaviors can also be transmitted across multiple generations through non-genetic factors, as recently reviewed (Bohacek and Mansuy, 2015).

  • Fetal exposure to teratogens: Evidence of genes involved in autism

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    Thalidomide might interact with a receptor or intracellular molecules that remain to be identified. It might also interact directly with DNA leading to modifications of the normal pattern of DNA methylation, and consequently to modifications of gene expression (Holliday, 1998; Huang and McBride, 1997). A recent study showed that a teratogenic dose of thalidomide (20 mg/kg) changes global gene expression profiles in the monkey embryo on day 26 of gestation (Ema et al., 2010).

  • Epigenetic effects of endocrine-disrupting chemicals on female reproduction: An ovarian perspective

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    Although molecular mechanisms remain to be detailed, these observations suggest that effects of environment are transmitted between generations via epigenetic (non-Mendelian) inheritance [260]. For over two decades, scientists have considered the possibility that epigenetic changes in the germline induced by exogenous factors can be inherited [131,132]. Mitotic inheritance of the epigenetic marks was discussed in Section 2.1.1, and meiotic inheritance is described as follows.

  • Epigenetic transgenerational actions of environmental factors in disease etiology

    2010, Trends in Endocrinology and Metabolism
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    Holliday initially proposed a link between hormone action and establishment of DNA methylation in mammalian embryos. He proposed that maternal effects of teratogens might disrupt the normal distribution of DNA methylation in a developing embryo, leading to developmental abnormalities or defects that would appear in successive generations [58]. McLachlan and collaborators [59] proposed that exposure to environmental endocrine disrupting chemicals during early development affects adult stages, potentially involving gene imprinting and leading to persistent genetic change at the level of DNA methylation.

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