Phenylpyrazole insecticides induce cytotoxicity by altering mechanisms involved in cellular energy supply in the human epithelial cell model Caco-2
| Autor: | Jean-Luc Brunet, Alexandra Badiou, Cyril Vidau, Luc P. Belzunces |
|---|---|
| Přispěvatelé: | Abeilles et Environnement (AE), Institut National de la Recherche Agronomique (INRA)-Avignon Université (AU) |
| Rok vydání: | 2009 |
| Předmět: |
Insecticides
CACO-2 CELL LDH [SDV]Life Sciences [q-bio] FIPRONIL ENERGETIC METABILISM Biology Toxicology INTESTINAL EPITHELIUM EPITHELIUM INTESTINAL chemistry.chemical_compound Adenosine Triphosphate SULFONE SULFIDE Electric Impedance Humans CYTOTOXICITY Lactic Acid Viability assay PHENYLPYRAZOLE Cytotoxicity TEER Barrier function Fipronil Cell Proliferation Dose-Response Relationship Drug L-Lactate Dehydrogenase TRANSEPITHELIAL ELECTRIC RESISTANCE LACTATE DEHYDROGENASE HUMAN Epithelial Cells CELLULE CACO-2 General Medicine Metabolism ETHIPROL Intestinal epithelium Mitochondria ATP METABOLITE INTESTIN Biochemistry chemistry INSECTICIDE Caco-2 CYTOTOXICITE Pyrazoles Caco-2 Cells Energy Metabolism Xenobiotic |
| Zdroj: | Toxicology in Vitro Toxicology in Vitro, Elsevier, 2009, 23, pp.589-597. ⟨10.1016/j.tiv.2009.01.017⟩ |
| ISSN: | 0887-2333 |
| DOI: | 10.1016/j.tiv.2009.01.017 |
| Popis: | Phenylpyrazoles are relatively new insecticides designed to manage problematic insect resistance and public health hazards encountered with older pesticide families. In vitro cytotoxicity induced by the phenylpyrazole insecticides, Ethiprol and Fipronil, and Fipronil metabolites, sulfone and sulfide, was studied in Caco-2 cells. This cellular model was chosen because it made possible to mimic the primary site of oral exposure to xenobiotics, the intestinal epithelium. Assessment of the barrier function of Caco-2 epithelium was assessed by TEER measurement and showed a major loss of barrier integrity after exposure to Fipronil and its metabolites, but not to Ethiprol. The disruption of the epithelial barrier was attributed to severe ATP depletion independent of cell viability, as revealed by LDH release. The origin of energetic metabolism failure was investigated and revealed a transient enhancement of tetrazolium salt reduction and an increase in lactate production by Caco-2 cells, suggesting an increase in glucose metabolism by pesticides. Cellular symptoms observed in these experiments lead us to hypothesize that phenylpyrazole insecticides interacted with mitochondria |
| Databáze: | OpenAIRE |
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