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Apoptotic and proliferative activity of mouse gastric mucosa following oral administration of fumonisin B1
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: Twe...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Mashhad University of Medical Sciences
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4366747/ https://www.ncbi.nlm.nih.gov/pubmed/25810870 |
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author | Alizadeh, Ali Mohammad Mohammadghasemi, Fahimeh Zendehdel, Kazem Kamyabi-moghaddam, Zahra Tavassoli, Abbas Amini-najafi, Fatemeh Khosravi, Alireza |
author_facet | Alizadeh, Ali Mohammad Mohammadghasemi, Fahimeh Zendehdel, Kazem Kamyabi-moghaddam, Zahra Tavassoli, Abbas Amini-najafi, Fatemeh Khosravi, Alireza |
author_sort | Alizadeh, Ali Mohammad |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-4366747 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Mashhad University of Medical Sciences |
record_format | MEDLINE/PubMed |
spelling | pubmed-43667472015-03-25 Apoptotic and proliferative activity of mouse gastric mucosa following oral administration of fumonisin B1 Alizadeh, Ali Mohammad Mohammadghasemi, Fahimeh Zendehdel, Kazem Kamyabi-moghaddam, Zahra Tavassoli, Abbas Amini-najafi, Fatemeh Khosravi, Alireza Iran J Basic Med Sci Original Article 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. Mashhad University of Medical Sciences 2015-01 /pmc/articles/PMC4366747/ /pubmed/25810870 Text en Copyright: © Iranian Journal of Basic Medical Sciences http://creativecommons.org/licenses/by-nc-sa/3.0 This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Alizadeh, Ali Mohammad Mohammadghasemi, Fahimeh Zendehdel, Kazem Kamyabi-moghaddam, Zahra Tavassoli, Abbas Amini-najafi, Fatemeh Khosravi, Alireza Apoptotic and proliferative activity of mouse gastric mucosa following oral administration of fumonisin B1 |
title | Apoptotic and proliferative activity of mouse gastric mucosa following oral administration of fumonisin B1 |
title_full | Apoptotic and proliferative activity of mouse gastric mucosa following oral administration of fumonisin B1 |
title_fullStr | Apoptotic and proliferative activity of mouse gastric mucosa following oral administration of fumonisin B1 |
title_full_unstemmed | Apoptotic and proliferative activity of mouse gastric mucosa following oral administration of fumonisin B1 |
title_short | Apoptotic and proliferative activity of mouse gastric mucosa following oral administration of fumonisin B1 |
title_sort | apoptotic and proliferative activity of mouse gastric mucosa following oral administration of fumonisin b1 |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4366747/ https://www.ncbi.nlm.nih.gov/pubmed/25810870 |
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