Tebuconazole Fungicide Induces Lipid Accumulation and Oxidative Stress in HepG2 Cells
Autor: | Dong-Min Shin, Dong-Wook Kim, Hyuk-Cheol Kwon, Su-Jin Lim, Do Hyun Kim, Chang-Hee Jeong, Sung Gu Han, Yea-Ji Kim, Jong-Hyun Han |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
Health (social science)
tebuconazole TP1-1185 Plant Science medicine.disease_cause Health Professions (miscellaneous) Microbiology Article Microsomal triglyceride transfer protein chemistry.chemical_compound Carnitine palmitoyltransferase 1 lipid metabolism medicine oxidative stress Tebuconazole chemistry.chemical_classification biology Chemistry Chemical technology lipid accumulation Fatty liver Fatty acid non-alcoholic fatty liver disease Lipid metabolism Peroxisome medicine.disease Cell biology biology.protein Oxidative stress Food Science |
Zdroj: | Foods Volume 10 Issue 10 Foods, Vol 10, Iss 2242, p 2242 (2021) |
ISSN: | 2304-8158 |
DOI: | 10.3390/foods10102242 |
Popis: | 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. |
Databáze: | OpenAIRE |
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