Effects of aflatoxin B1 on mitochondrial respiration, ROS generation and apoptosis in broiler cardiomyocytes

Abstract Aflatoxin B1 ( AFB 1) develops various toxic effects in the liver by impairing mitochondrial function, inducing cell apoptosis. However, little is focused on its toxicity to broiler cardiomyocytes ( BCM s). Here, the mitochondrial membrane potential ( MMP ), reactive oxygen species ( ROS ) generation, cardiac troponin T ( cTnT ) location, apoptosis induced by AFB 1, and antioxidative genes were investigated in BCM s. It was found that AFB 1 evoked intracellular ROS generation, and induced apoptosis in BCM s. AFB 1 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 BCM s. These findings suggested AFB 1 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.