Author/Authors :
-، - نويسنده 1 Cancer Research Center, Tehran University of Medical Sciences, Tehran, Iran
2 Cancer Model Research Center, Tehran University of Medical Sciences, Tehran, Iran Alizadeh, Ali Mohammad , -، - نويسنده Cellular and Molecular Research Center, Faculty of Medicine, Guilan University of Medical Sciences, Rasht, Iran Mohammadghasemi, Fahimeh , -، - نويسنده Cancer Research Center, Tehran University of Medical Sciences, Tehran, Iran Zendehdel, Kazem , -، - نويسنده Department of Pathology, Faculty of Veterinary Medicine, Tehran University, Tehran, Iran Kamyabi-moghaddam, Zahra , -، - نويسنده Department of Pathology, Faculty of Veterinary Medicine, Tehran University, Tehran, Iran Tavassoli, Abbas , -، - نويسنده Department of Pathology, Faculty of Veterinary Medicine, Tehran University, Tehran, Iran najafi, Fatemeh Amini , -، - نويسنده Medical Parasitology and Mycology Department, School of Medicine, Tehran University, Tehran, Iran Khosravi, Alireza
Abstract :
Objective(s):Fumonisins are a group of toxic and carcinogenic mycotoxins, which contaminate the grains and their products. The aim of this study was to examine the apoptotic and proliferative activity of mouse gastric mucosa following administration of fumonisin B1 (FB1). Materials and Methods: Twenty-nine female mice divided into treatment (n=15) and control (n=14) groups. The treatment group received FB1 (150 mg/kg diet) for 16 weeks. The gastric atrophy was allocated using grading criteria modeled on the updated Sydney System. Immunohistochemistry studies were performed for evaluation of apoptosis and proliferative activity in gastric mucosa. Results: Mild to moderate gastric atrophy were observed in microscopic findings of the gastric mucosa in treated animals (P<0.05). Number of parietal cells significantly decreased in the treatment group in comparison with the control (P<0.05). Treatment with FB1 for 16 weeks significantly reduced both gastric mucosa height and mitotic index in the gastric glands (P<0.05). TUNEL- and Bax-labeled positive cell numbers significantly increased in the FB1-treated group compared to the control (P<0.05). In addition, proliferative activity of gastric glands in the treated group was significantly lower than the control (P<0.05). Conclusion: Oral administration of FB1 caused atrophy in gastric mucosa both via increasing of apoptosis and suppressing the mitotic activity of these cells.
