The Influence of Aflatoxin B1 on the Concentration of Nuclear Factor κB in Rats’ Livers

Introduction. Aflatoxins are metabolites produced by Aspergillus flavus and Aspergillus parasiticus. Due to the high prevalence of aflatoxin-containing products they are common issue of the observational studies. Observational studies have demonstrated the hepatotoxic effects of aflatoxins in humans. However, the exact pathogenetic mechanisms of the effect of aflatoxin B1 on the above-mentioned hepatotoxicity have not yet been known.

Aim of the study. The aim of the study was to assess the toxic effects of different doses of aflatoxin B1. The analyze was performed using assessment of concentration of NF-κB in liver tissue homogenates after a 7-day intoxication with this mycotoxin.

Material and methods. The studies were carried out on Wistar male rats which were selected randomly, according to the principle of simultaneity for the control group and the study groups. The concentration of NK-κB was determined by immunoenzymatic ELISA in the obtained supernatants of liver taken from decapitated animals. The statistical analysis was performed with Statistica 13.3 (Statsoft, USA).

Results. The statistical significance of the difference between the concentrations in the control and study group receiving 1.0 mg/kg of aflatoxin B1 and between the control and study group who received aflatoxin B1 at a dose of 2.0 mg/kg body weight (p <0,05) were demonstrated. A significant relationship was also found between the level of dose of aflatoxin B1 administered to the rats and the concentration of NF-κB. Negative correlations were obtained. The higher dose administered to rats - the lower level of measured concentration of NF-κB.

Conclusions. The study of the influence of aflatoxin B1 on the level of NF-κB transcription factor may significantly contribute to understand the mechanism of its action, influence on inflammatory, apoptotic and carcinogenic processes in the liver and determine its safe level in food intended for humans and animals.