Aflatoxin B1 is highly hepatotoxic & carcinogenic
Sterigmatocystin is enzymatically
converted into Aflatoxin B1,
both are bisfuranomethoxybenzenes
from Singh R., Appl. and Environ. Microbiol. 1976 (31) 743
Aflatoxins illustrate that food is an essential source of a carcinogenic mycotoxin.
Sterigmatocystin is its "water damage" counterpart, but can be transformed into Aflatoxin
Primary liver cancers are increasing
at a high rate
Sterigmatocystin is in category 2B, Aflatoxin is in category 1
Aflatoxin can kill before inducing cancer, as shown in this child:
Prior hepatitis B or C infection facilitates Aflatoxin carcinogenesis.
Key sources: peanuts, corn (maize), rice
and cassava (manioc)
Carcinogenicity of occupational exposure to Aflatoxin is demonstrated. In Denmark cancer risk was evaluated in male employees of 279 livestock feed processing companies (mean aflatoxin concentration 10 - 60 microg/Kg); Work consisted in unloading of ships, processing and packaging into sacks. Exposed workers may have inhaled 170 ng aflatoxin B1 per day. SPIR ( standardized proportional incidence ratio, SPIR) is the ratio of observed incidence of cancer at one specific anatomical site among employees of these companies, to the incidence for all employees in Denmark.Olsen, Br. J. Cancer, 1988, 58: 392;
p not measured as N < 5 in both groups
average daily dietary intake
Huantai townships are at low risk of hepatocarcinoma (HC) or esophageal cancer (EC)
Huaian townships are at high risk of ESOPHAGEAL cancer: high FB1 intake
Fusui townships are at high risk of hepatocarcinoma: high AFB1 intake
Sun G; et al; Food Addit. Contam.2011; 28: 461
Correlation between average daily intake of
Aflatoxin and high risk of hepatocarcinoma
Every year, around 100,000 new cases of hepatocellular carcinoma, practically always fatal, are attributable to Aflatoxin exposure (from Liu Y et al;, Env. Health Perspectives 2010, 118: 818)
Three main biological issues are involved in Aflatoxin carcinogenicity:
- Somatic mutations in the p53 tumor suppressor gene (TP53), with induction of G:C to T:A transversions in codon 249 of TP53.
- Development of DNA adducts, bound to Aflatoxin epoxides.