Aflatoxin B1 induces reactive oxygen species-dependent caspase-mediated apoptosis in normal human cells, inhibits Allium cepa root cell division, and triggers inflammatory response in zebrafish larvae

Mycotoxin contamination of food and water is a serious global concern. Aflatoxin B1 (AFB1) is a deadly mycotoxin that contaminates both food and water bodies in the environment. AFB1 is reported to cause severe health issues, including hepatotoxicity, teratogenicity, and immunotoxicity in humans; however, the mechanistic effects on plant and aquatic animals are not fully understood. To obtain a clear understanding of the effects of AFB1 on the ecosystem, we examined the influence of AFB1 exposure on different model systems corresponding to various habitats. In the current study, AFB1 contamination consequences were studied on a human normal cell lines (HaCaT, CCD 841 CoN), meristematic Allitun cepa (onion) root cells, and zebrafish embryonic development. Our results clearly indicate that concentrations of AFB1 >10 mu M are toxic to HaCaT cells. Morphological changes of HaCaTand CCD 841 CoN cells were clearly observed after exposure to AFB1. Particularly in HaCaT cells, treatment with 50 mu M and 100 mu M AFB1induces oxidative stress by excessive endogenous free-radical production such as ROS and NO generation. These consequences accelerate the ROS-dependent DNA damage events, which subsequently result in caspase mediated programmed cell death. Exposure of A. cepa root cells to AFB1 for 24 h resulted in abnormal cell division. A. cepa root cells subjected to AFB1 treatment showed a significant concentrationdependent increase in metaphase arrest. Exposure of zebrafish embryos to AFB1 also revealed that AFB1 contamination restricts the larval growth and development, resulting in a remarkably increased zebrafish mortality rate. Collectively, results of the current study indicate that AFB1 contamination triggers the programmed cell death machinery, subsequently affecting the ecosystem. (C) 2020 Elsevier B.V. All rights reserved.