Chlorpyrifos pesticide promotes oxidative stress and increases inflammatory states in BV-2 microglial cells: A role in neuroinflammation
| Autor: | Ivana Beatrice Mânica da Cruz, Cinthia Melazzo de Andrade, Micheli M. Pillat, Charles Elias Assmann, Maria Rosa Chitolina Schetinger, Jéssica Righi da Rosa, Vitor Bastianello Mostardeiro, Grazielle Castagna Cezimbra Weis, Vera Maria Morsch, Ijoni Hilda Costabeber, Audrei de Oliveira Alves |
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| Rok vydání: | 2021 |
| Předmět: |
Insecticides
Environmental Engineering Health Toxicology and Mutagenesis 0208 environmental biotechnology Inflammation 02 engineering and technology 010501 environmental sciences Pharmacology medicine.disease_cause 01 natural sciences Mice chemistry.chemical_compound Immune system medicine Animals Environmental Chemistry Pesticides Neuroinflammation 0105 earth and related environmental sciences biology Organophosphate Public Health Environmental and Occupational Health Neurotoxicity General Medicine General Chemistry medicine.disease Pollution 020801 environmental engineering Oxidative Stress chemistry Integrin alpha M Chlorpyrifos biology.protein Microglia medicine.symptom Oxidative stress |
| Zdroj: | Chemosphere. 278:130417 |
| ISSN: | 0045-6535 |
| Popis: | The exposure to environmental stressors, such as organophosphate (OP) pesticides, has been associated with the development of neurodegenerative diseases. Chlorpyrifos (CPF) is the worldwide most used OP pesticide and one of the most hazardous pesticides as it can cross the blood-brain barrier. Since studies evaluating the effects of CPF on brain immune cells are scarce, this research investigated the oxidative and inflammatory responses of CPF exposure in murine microglial cells. BV-2 cells were exposed to different concentrations of CPF pesticide (0.3–300 μM). CPF induced activation of microglial cells, confirmed by Iba-1 and CD11b marking, and promoted microglial proliferation and cell cycle arrest at S phase. Moreover, CPF exposure increased oxidative stress production (NO, MDA, and O2∙), and upregulated pro-inflammatory cytokines (IL-1β and NLRP3) genes expression in BV-2 cells. Overall, data showed that CPF exposure, at the lowest concentrations, acted by promoting pro-oxidative and pro-inflammatory states in microglial cells. These results provide important information on the potential role of microglial activation in CPF-induced neuroinflammation and add to the expanding knowledge on the neurotoxicity of OP. |
| Databáze: | OpenAIRE |
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