This is in contrast to the recently reported lack of methylation changes after exposure of hESCs to 20 mM EtOH (Krishnamoorthy et al., 2013). Interestingly, their reported selective gene subsets are, for the most part, also unchanged in our study, whereas the much larger set of genes which do show methylation changes in our study are not reported by these authors. Furthermore, numerous studies have linked epigenetic mechanisms as potential regulatory events involved in alcohol teratogenesis (Bielawski et al., 2002; Garro et al., 1991; Haycock, 2009; Kaminen-Ahola et al., 2010). Epigenetic imprinting or genome-wide epigenetic reprogramming has been proposed as a mechanism responsible for alcohol-induced teratogenesis in preimplantation embryos (Haycock, 2009; Haycock and Ramsay, 2009). Interestingly, even paternal or maternal alcohol consumption prior to conception has been shown to result in a wide range of birth defects and fetal abnormalities. It is likely that alcohol-induced epigenetic changes in the gametes or within germ line are responsible for pre-conceptional effects of alcohol (Abel, 2004).
