Aflatoxins are poisonous by-products from the fungus Aspergillus, with aflatoxin B1 (AFB1) being the most toxic. Very high concentrations of aflatoxins are found in nutritive seeds like maize, nuts, cereal grains, and rice. They have been implicated in many gastrointestinal and hepatic diseases. Studies on their effects on the pancreas are limited. Phenolic antioxidants like butylated hydroxytoluene (BHT) were reported to be chemoprotective against aflatoxicosis in some animal models.Aim
This work aimed to demonstrate the histopathological effects of chronic AFB1 toxicity on the exocrine and endocrine pancreas and evaluate the possible protective role of BHT in these structural changes.Materials and methods
Thirty adult male albino rats were randomly divided into three groups: group I served as the control group; group II received 60 µg/kg of AFB1 orally three times weekly for 5 consecutive weeks; and group III received a concomitant dose of BHT (0.05 mg/kg) orally along with AFB1. After the rats had been sacrificed, pancreatic specimens were taken and processed for histological, immunohistochemical, and morphometric study.Results
Both exocrine and endocrine pancreas of group II showed marked degenerative changes. Acinar cells exhibited decreased or almost absent basal basophilia and reduced content of zymogen granules in periodic acid Schiff-stained sections. Periductal and perivascular fibrosis was observed with dilatation and congestion of blood vessels and inflammatory cell infiltration. β-Cells were degenerated and expressed decreased insulin immunostaining. There was significant decrease in islet surface area, islet diameter, islet volume, and numerical density of β-cells compared with the control group. The pancreas of group III showed marked improvement compared with the aflatoxicosed group.Conclusion
Treatment with AFB1 for 5 weeks has a direct toxic effect on the exocrine and endocrine pancreas that can ultimately affect its performance. The use of BHT markedly attenuates these effects and can be considered an effective chemoprotective agent against AFB1 toxicity.