The molecular mechanism of G(2)/M cell cycle arrest induced by AFB(1) in the jejunum

Aflatoxin B(1) (AFB(1)) has potent hepatotoxic, carcinogenic, genotoxic, immunotoxic and other adverse effects in human and animals. The aim of this study was to investigate the molecular mechanism of G(2)/M cell cycle arrest induced by AFB(1) in the jejunum of broilers. Broilers, as experimental an...

Descripción completa

Detalles Bibliográficos
Autores principales: Yin, Heng, Jiang, Min, Peng, Xi, Cui, Hengmin, Zhou, Yi, He, Min, Zuo, Zhicai, Ouyang, Ping, Fan, Junde, Fang, Jing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2016
Materias:
Research Paper: Pathology
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5094947/
https://www.ncbi.nlm.nih.gov/pubmed/27232757
http://dx.doi.org/10.18632/oncotarget.9594
Descripción
Sumario:Aflatoxin B(1) (AFB(1)) has potent hepatotoxic, carcinogenic, genotoxic, immunotoxic and other adverse effects in human and animals. The aim of this study was to investigate the molecular mechanism of G(2)/M cell cycle arrest induced by AFB(1) in the jejunum of broilers. Broilers, as experimental animals, were fed 0.6 mg/kg AFB(1) diet for 3 weeks. Our results showed that AFB(1) reduced the jejunal villus height, villus height/crypt ratio and caused G(2)/M cell cycle arrest. The G(2)/M cell cycle was accompanied by the increase of ataxia telangiectasia mutated (ATM), p53, Chk2, p21 protein and mRNA expression, and the decrease of Mdm2, cdc25C, cdc2, cyclin B and proliferating cell nuclear antigen protein and mRNA expression. In conclusion, AFB(1) blocked G(2)/M cell cycle by ATM pathway in the jejunum of broilers.

Ejemplares similares