ABSTRACT
Aflatoxins are a group of highly toxic metabolites, studied primarily because of their negative effects on human health. They represent food contaminants, produced by strains of fungi, such as Aspergillus flavus and A. parasiticus. Among them aflatoxin B1 (AFB1) is the most frequent food contaminant and the major target of AFB1 toxicity is the liver. A large number of studies on aflatoxins have been undertaken with the aim of identifying the mechanism of their toxicity and eventually designing appropriate protocols for the removal of the toxic derivatives from contaminated food. AFB1 exposure causes alteration of several specific cellular activities; among these, impairment of the cell cycle progression mechanism appears particularly relevant, considering the carcinogenetic action of the toxin. Direct analysis of AFB1 effects on cell cycle progression has been performed on cell lines; the results of this study point to a role for p53 in the response to AFB1. Considerable attention has been dedicated to investigation of the interference of AFB1 with molecular components of cell cycle checkpoints. These studies are reviewed; they strongly suggest that p53, p27, p16, and p19 functions are impaired by AFB1. DNA methylation appears to be a major mechanism for cell cycle inhibitory control inactivation.
