Effects of aflatoxin B1 on mitochondrial respiration, ROS generation and apoptosis in broiler cardiomyocytes.
Anim Sci J
; 88(10): 1561-1568, 2017 Oct.
Article
en En
| MEDLINE
| ID: mdl-28401999
ABSTRACT
Aflatoxin B1 (AFB1) develops various toxic effects in the liver by impairing mitochondrial function, inducing cell apoptosis. However, little is focused on its toxicity to broiler cardiomyocytes (BCMs). Here, the mitochondrial membrane potential (MMP), reactive oxygen species (ROS) generation, cardiac troponin T (cTnT) location, apoptosis induced by AFB1, and antioxidative genes were investigated in BCMs. It was found that AFB1 evoked intracellular ROS generation, and induced apoptosis in BCMs. AFB1 treatment resulted in increased percentage of apoptotic cells, increased location range of cTnT in cytoplasm, upregulated messenger RNA (mRNA) expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and downregulated mRNA expressions of Mn-superoxide dismutase in BCMs. These findings suggested AFB1 treatment caused significant cardiomyocyte damage and cardiotoxicity, impairment of mitochondrial functions, activated ROS generation, and induced apoptosis, and probably was involved in the Nrf2 signal pathway in BCMs.
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Base de datos:
MEDLINE
Asunto principal:
Aflatoxina B1
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Especies Reactivas de Oxígeno
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Apoptosis
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Miocitos Cardíacos
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Potencial de la Membrana Mitocondrial
Idioma:
En
Revista:
Anim Sci J
Asunto de la revista:
MEDICINA VETERINARIA
Año:
2017
Tipo del documento:
Article