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Bifenthrin is one of the widely used synthetic pyrethroid insecticides, employed for various purposes worldwide. As lipophilic pyrethroids can easily bind to soil particles, which is why their residues are detected in various environments. Consequently, the toxicity of bifenthrin to non-target organisms can be regarded as an environmental concern. The toxic effects of bifenthrin have been studied in various animal models and cell lines; however, its toxic effects on cattle remain unclear. In particular, gaining insights into the toxic effects of bifenthrin on the mammary lactation system is crucial for the dairy industry. Therefore, we proceeded to investigate the toxic effects of bifenthrin on the bovine mammary epithelial cells (MAC-T cells). We established that bifenthrin inhibited cell proliferation and triggered apoptosis in MAC-T cells. Additionally, bifenthrin induced mitochondrial dysfunction and altered inflammatory gene expression by disrupting mitochondrial membrane potential (MMP) and generating excessive reactive oxygen species (ROS). We also demonstrated that bifenthrin disrupted both cytosolic and mitochondrial calcium ion homeostasis. Furthermore, bifenthrin altered mitogen-activated protein kinase (MAPK) signaling cascades and downregulated casein-related genes. Collectively, we confirmed the multiple toxic effects of bifenthrin on MAC-T cells, which could potentially reduce milk yield and quality. Copyright © 2023 Elsevier Inc. All rights reserved.


Eunho Sung, Junho Park, Hojun Lee, Gwonhwa Song, Whasun Lim. Bifenthrin induces cell death in bovine mammary epithelial cells via ROS generation, calcium ion homeostasis disruption, and MAPK signaling cascade alteration. Pesticide biochemistry and physiology. 2023 Nov;196:105637

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PMID: 37945236

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