Aflatoxin B1 (AFB1) is currently the most commonly studied mycotoxin due to its great
toxicity, its distribution in a wide variety of foods such as grains and cereals and
its involvement in the development of + (hepatocellular carcinoma; HCC). HCC is one
of the main types of liver cancer, and has become a serious public health problem,
due to its high incidence mainly in Southeast Asia and Africa. Studies show that AFB1
acts in synergy with other risk factors such as hepatitis B and C virus leading to
the development of HCC through genetic and epigenetic modifications. The genetic modifications
begin in the liver through the biomorphic AFB1, the AFB1-exo-8.9-Epoxy active, which
interacts with DNA to form adducts of AFB1-DNA. These adducts induce mutation in codon
249, mediated by a transversion of G–T in the p53 tumor suppressor gene, causing HCC.
Thus, this review provides an overview of the evidence for AFB1-induced epigenetic
alterations and the potential mechanisms involved in the development of HCC, focusing
on a critical analysis of the importance of severe legislation in the detection of
aflatoxins.
Abbreviations:
AFB1 (Aflatoxin B1), AFM1 (Aflatoxin M1), AVF (averufin), AVN (averantine), AVNN (averufanin), CYP450 (cytochrome P450), DHDMST (dihydrodemethylsterigmatocystin), DHOMST (dihydro-O-methylsterigmatocystin), DNMT (DNA methyltransferases), HATs (histone acetyltransferases), HAVN (5′hydroxy averantine), HCC (hepatocarcinoma), HDACs (histone deacetylases enzymes), IL-1 (interleukin-1), IL-6 (interleukin-6), JAK (Janus kinases), NOR (norsolorinic acid), OMST (O-methylsterigmatocystin), ST (sterigmatocystin), TNF-α (tumor necrosis factor), VAL (versiconal), VER B (versicolorin B), VHA (versiconal hemiacetal acetate), STAT (signal transducer and activator of transcription), Wnt (Wnt family), HBc (Hepatitis B core), CG (guanine-cytosine), PCR (Polymerase Chain Reaction), ALFs (aflatoxins)To read this article in full you will need to make a payment
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Article info
Publication history
Published online: September 14, 2018
Accepted:
September 2,
2018
Received in revised form:
August 27,
2018
Received:
May 9,
2018
Identification
Copyright
© 2018 Elsevier Inc. All rights reserved.
