Fumonisin B1 actuates oxidative stress‐associated colonic damage via apoptosis and autophagy activation in murine model

In the present study, we investigated the cytotoxic mechanism of Fumonisin B1 (FB1) in mice colonic region in a time course manner. Herein, after consecutive 4 days of exposure to FBI (2.5 mg/kg body weight), we observed disintegration of mice colon, as evidenced by histopathological analysis. FB1 s...

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Bibliographic Details
Published in:Journal of biochemical and molecular toxicology 2018-07, Vol.32 (7), p.e22161-n/a
Main Authors: Kim, Sang Ho, Singh, Mahendra Pal, Sharma, Chanchal, Kang, Sun Chul
Format: Article
Language:English
Subjects:
Activation
Alanine
Alanine transaminase
Alkaline phosphatase
Animal models
Antioxidants
Apoptosis
Aspartate aminotransferase
Autophagy
Body weight
Cell death
Ceramide
Colon
Cytotoxicity
Disintegration
ER stress
Fumonisin B1
Kinases
Mice
Oxidative stress
Peroxidase
Phagocytosis
Protein kinase C
Proteins
Sphinganine
Toxicity
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Summary:In the present study, we investigated the cytotoxic mechanism of Fumonisin B1 (FB1) in mice colonic region in a time course manner. Herein, after consecutive 4 days of exposure to FBI (2.5 mg/kg body weight), we observed disintegration of mice colon, as evidenced by histopathological analysis. FB1 significantly increased alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase activities in serum and plasma, decreased ceramide level, increased sphinganine level, and increased lipid peroxidase level along with the breakdown of the antioxidant system. Further, FB1‐induced ER stress caused apoptosis and autophagy activation in mice colon, evidenced by increased expression of IRE1‐α, p‐JNK, Casp3, and LC3I/II. In addition, we also noticed a reduced protein kinase C expression in mice colon exposed to FB1, suggesting its role in ER stress‐induced cell death. Taken together, study suggests both physiologically and biochemically, FB1 toxicity to mice colon induced by oxidative stress‐associated apoptosis and autophagy activation.
ISSN:1095-6670
1099-0461
DOI:10.1002/jbt.22161