A growing body of evidence has implicated on the role of environmental exposures, particularly in early development, in the induction of epigenetic changes that may be transmitted to subsequent generations or may selleckchem serve as a basis of diseases

developed later in life. Furthermore, it has become so likely that epigenetics contribute to the causes or transmission of chronic disorders from one generation to another (Weinhold, 2006) (Fig. 2). Several evidence collected from animal studies during the past decade suggested that exposure to pesticides can induce epigenetic changes. Heritable alterations of DNA methylation in male germline along with testis and ovarian dysfunction have been reported after exposure to some pesticides like vinclozolin and methoxychlor (Anway and Skinner, 2006, Anway et al., 2005, Guerrero-Bosagna et al., 2010 and Zama and Uzumcu, 2009). Exposure to dichloroacetic acid and trichloroacetic acid has been associated with decreased methylation in promoter regions of c-jun and c-myc in liver of mice ( Tao et al., 2000a and Tao et al., 2000b). Global

DNA hypomethylation has also been reported in people who had an elevated blood level of pesticides and persistent organic pollutants in two surveys ( Kim et al., 2010 and Rusiecki et al., 2008). Furthermore, increased acetylation of core histones H3 and H4 has been reported by dieldrin, an organochlorine pesticide, in mouse models ( Song et al., 2010). On the other hand, growing progress has been made in the recognition of epigenetic modifications in human chronic diseases, particularly learn more cancer. Cancer is now considered as an epigenetic disease the same as a genetic disease. There is tremendous evidence on the contribution of epigenetic events in the initiation, promotion

and progression of different types of cancers, Buspirone HCl mainly through silencing of tumor suppressor genes and/or activation of proto-oncogenes. These modifications have allocated such a fundamental role in cancer development that epigenetic therapy of cancer is rapidly growing in medical sciences (Jones and Baylin, 2002). In addition, epigenetic changes currently have been a powerful tool for studying the carcinogenesis mechanisms of occupational and environmental exposures (Ziech et al., 2010). The first note on pesticide-induced carcinogenesis through epigenetic mechanisms was from a study carried out by Maslansky and colleagues in 1981. They reported hepatocarcinogenesis of organochlorine pesticides with no genotoxic effects in hepatocytes and suspected to epigenetic modifications disrupting intracellular communications (Maslansky and Williams, 1981). Later, reports presented about epigenetic actions of vinclozolin, a fungicide known to be an environmental endocrine disruptor, in association with adult-onset diseases, particularly tumor development (Skinner and Anway, 2007).