ArticleFoods (Basel, Switzerland)2021
Tebuconazole Fungicide Induces Lipid Accumulation and Oxidative Stress in HepG2 Cells.
Article in Foods (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- Hexaconazole-Induced Male Reproductive Toxicity Through ROS-Mediated Ferroptosis and Impaired Leydig Cell Steroidogenesis.International journal of molecular sciences · 2026Article
- Mechanism-based new approach methodologies for in vitro detection of chemical-induced liver steatosis.Archives of toxicology · 2026Review
- A Systematic Review on the Toxicology of European Union-Approved Triazole Fungicides in Cell Lines and Mammalian Models.Journal of xenobiotics · 2025Review
- Rice Protein Reduces Triglyceride Levels through Modulating CD36, MTP, FATP, and FABP Expression in Growing and Adult Rats.Foods (Basel, Switzerland) · 2024Article
- Metabolic pathway of tebuconazole by soil fungus Cunninghamella elegans ATCC36112.Antonie van Leeuwenhoek · 2023Article
- Tebuconazole Induces ER-Stress-Mediated Cell Death in Bovine Mammary Epithelial Cell Lines.Toxics · 2023Article
- Myclobutanil-mediated alteration of liver-gut FXR signaling in mice.Toxicological sciences : an official journal of the Society of Toxicology · 2023Article
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Authors and funding
9 authors at 2 institutions in 1 country.
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Abstract
Tebuconazole (TEB), a triazole fungicide, is frequently applied to agriculture for the increase of food production. Although TEB causes liver toxicity, its effects on cellular lipid accumulation are rarely investigated. Therefore, this study aimed to study the effects of TEB on lipid metabolism and accumulation in HepG2 cells. HepG2 cells were exposed to 0-320 µM TEB for 1-24 h. TEB (20-80 µM, 24 h)-treated cells showed lipid accumulation. Further, TEB (20-80 µM, 1-12 h) increased the nuclear translocation of peroxisome proliferator-activated receptors and the expression of lipid uptake and oxidation-related markers such as cluster of differentiation 36, fatty acid transport protein (FATP) 2, FATP5, and carnitine palmitoyltransferase 1. Oxidative stress levels in TEB-treated cells (20-80 µM, 24 h) were higher, compared to those in the control. TEB (20-80 µM, 24 h) also induced the loss of mitochondrial membrane potential and lower levels of microsomal triglyceride transfer protein in the cells. Thus, TEB can induce lipid accumulation by altering the expression of lipid-metabolizing molecules and can therefore impair lipid metabolism. Our data suggest that human exposure to TEB may be a risk factor for non-alcoholic fatty liver disease.
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Registered trials
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