Global DNA methylation in a population with aflatoxin B₁exposure

Abstract

(2013) Global DNA methylation in a population with aflatoxin B 1 exposure, Epigenetics, 8:9,[962][963][964][965][966][967][968][969]

Epigenetic alterations induced by genotoxic occupational and environmental human chemical carcinogens: A systematic literature review

“…The level of GSTP1 mRNA was inversely associated with promoter hypermethylation in a majority of the tumor samples, and a loss of this detoxifying enzyme that is involved in xenobiotic metabolism may be related to the associated DNA damage also observed in the tumors in this study. In addition to the site-specific gene methylation, hypomethylation of repetitive DNA elements, a characteristic indicative of genomic instability, has also been reported as a result of AFB1 exposure in both HCC and cancer-free patients with confirmed AFB1 exposure [92, 93]. …”

Epigenetic Signatures as Biomarkers of Exposure

“…In fact, changes in DNA methylation (DNAm), non-coding RNAs, and histone tail modifications have all been shown to be associated with human environmental exposures across a wide range of domains including toxicant, social/behavioral, diet, and pharmacologic. DNA methylation has been shown to undergo both losses and gains in global and/or repetitive elements with exposure to metals [1][2][3], benzene [4], persistent organic pollutants [5,6], particulate matter [7,8], mycotoxin [9], endocrine-disrupting chemicals [10], lifestyle factors [11,12], and inorganic arsenic [13,14]. In addition, locus-specific differences in DNAm associated with exposure to nutrition [15][16][17], inorganic arsenic [18,19], medications [20,21], childhood abuse [22] and stress [23], socioeconomic status [24,25], tobacco [26-32, 33•, 34, 35•, 36], polycyclic aromatic hydrocarbons [37,38], infections [39,40], and endocrine-disrupting chemicals [41,42] have also been observed.…”

Sequential dietary exposure to aflatoxin B1 and fumonisin B1 in F344 rats increases liver preneoplastic changes indicative of a synergistic interaction

“…AFB 1 induced liver cancer is characterized by a G to T mutation at codon 249 of the p53 gene (Aguilar et al, 1993) and possibly epigenetic effects involving DNA methylation (Wu et al, 2013). On the other hand, FB 1 induces cancer in rodents and trout through the disruption of sphingolipid metabolism via inhibition of ceramide synthase leading to alterations of key signaling pathways, induction of oxidative damage, and alterations in growth regulation (Bulder, 2012; Gelderblom et al, 2001a; IARC, 2002; Merrill et al, 2001; Riedel et al, 2015; Riley et al, 2001).…”