Epigenetic alterations caused by aflatoxin b1: a public health risk in the induction of hepatocellular carcinoma

Transl Res. 2019 Feb:204:51-71. doi: 10.1016/j.trsl.2018.09.001. Epub 2018 Sep 15.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Aflatoxin B1 / toxicity*
  • Carcinoma, Hepatocellular / chemically induced*
  • Carcinoma, Hepatocellular / genetics
  • DNA Methylation
  • Epigenesis, Genetic / drug effects*
  • Histones / metabolism
  • Humans
  • Liver Neoplasms / chemically induced*
  • Liver Neoplasms / genetics
  • MicroRNAs / physiology
  • Protein Biosynthesis
  • Public Health*
  • RNA, Long Noncoding / physiology
  • Risk

Substances

  • Histones
  • MicroRNAs
  • RNA, Long Noncoding
  • Aflatoxin B1