Aflatoxin - Pathology

Pathology

High-level aflatoxin exposure produces an acute hepatic necrosis, resulting later in cirrhosis, and/or carcinoma of the liver. Acute hepatic failure is made manifest by hemorrhage, edema, alteration in digestion, changes to the absorption and/or metabolism of nutrients, and mental changes and/or coma.

No animal species is immune to the acute toxic effects of aflatoxins; however, adult humans have a high tolerance for aflatoxin exposure and rarely succumb to acute aflatoxicosis.

Chronic, subclinical exposure does not lead to symptoms as dramatic as acute aflatoxicosis. Children, however, are particularly affected by aflatoxin exposure, which leads to stunted growth and delayed development. Chronic exposure also leads to a high risk of developing liver cancer, as aflatoxin metabolites can intercalate into DNA and alkylate the bases through its epoxide moiety. This is thought to cause mutations in the p53 gene, an important gene in preventing cell cycle progression when there are DNA mutations, or signaling apoptosis. These mutations seem to affect some base pair locations more than others — for example, the third base of codon 249 of the p53 gene appears to be more susceptible to aflatoxin-mediated mutations than nearby bases.

Medical research indicates that a regular diet including apiaceous vegetables such as carrots, parsnips, celery and parsley, reduces the carcinogenic effects of aflatoxin.

Moreover, aflatoxin B₁ can permeate through the skin. Dermal exposure to this aflatoxin in particular environmental conditions can lead to serious health risks.