| Autor: |
López-Aceves TG; Regional Graduate Program in Biotechnology, Faculty of Biological Chemical Sciences, Autonomous University of Sinaloa, Culiacán 80000, Mexico.; Laboratory of Neuroscience, National Institute of Pediatrics, Mexico City 04530, Mexico., Coballase-Urrutia E; Laboratory of Neuroscience, National Institute of Pediatrics, Mexico City 04530, Mexico., Estrada-Rojo F; Department of Physiology, Faculty of Medicine, National Autonomous University of Mexico, Mexico City 04510, Mexico., Vanoye-Carlo A; Laboratory of Neuroscience, National Institute of Pediatrics, Mexico City 04530, Mexico., Carmona-Aparicio L; Laboratory of Neuroscience, National Institute of Pediatrics, Mexico City 04530, Mexico., Hernández ME; Subdirection of Clinical Research, National Institute of Psychiatry, Mexico City 14370, Mexico., Pedraza-Chaverri J; Department of Biology, Faculty of Chemistry, National Autonomous University of Mexico, Mexico City 04150, Mexico., Navarro L; Department of Physiology, Faculty of Medicine, National Autonomous University of Mexico, Mexico City 04510, Mexico., Aparicio-Trejo OE; Department of Biology, Faculty of Chemistry, National Autonomous University of Mexico, Mexico City 04150, Mexico., Pérez-Torres A; Department of Cell and Tissue Biology, Faculty of Medicine, National Autonomous University of Mexico, Mexico City 04510, Mexico., Medina-Campos ON; Department of Biology, Faculty of Chemistry, National Autonomous University of Mexico, Mexico City 04150, Mexico., Martínez-Fong D; Department of Physiology, Biophysics and Neurosciences, Center for Research and Advanced Studies, Mexico City 07360, Mexico., Sánchez-Valle V; Neuroplasticity and Neurodegeneration Laboratory, Department of Pharmacology, Center for Research and Advanced Studies, Mexico City 07360, Mexico., Cárdenas-Rodríguez N; Laboratory of Neuroscience, National Institute of Pediatrics, Mexico City 04530, Mexico., Granados-Rojas L; Laboratory of Neuroscience, National Institute of Pediatrics, Mexico City 04530, Mexico., Pulido-Camarillo E; Department of Cell and Tissue Biology, Faculty of Medicine, National Autonomous University of Mexico, Mexico City 04510, Mexico., Rodríguez-Mata V; Department of Cell and Tissue Biology, Faculty of Medicine, National Autonomous University of Mexico, Mexico City 04510, Mexico., León-Sicairos CDR; Regional Graduate Program in Biotechnology, Faculty of Biological Chemical Sciences, Autonomous University of Sinaloa, Culiacán 80000, Mexico. |
| Abstrakt: |
Permethrin (PERM) is a member of the class I family of synthetic pyrethroids. Human use has shown that it affects different systems, with wide health dysfunctions. Our aim was to determine bioenergetics, neuroinflammation and morphology changes, as redox markers after subacute exposure to PERM in rats. We used MDA determination, protein carbonyl assay, mitochondrial O 2 consumption, expression of pro-inflammatory cytokines and a deep histopathological analysis of the hippocampus. PERM (150 mg/kg and 300 mg/kg body weight/day, o.v.) increased lipoperoxidation and carbonylated proteins in a dose-dependent manner in the brain regions. The activities of antioxidant enzymes glutathione peroxidase, reductase, S-transferase, catalase, and superoxide dismutase showed an increase in all the different brain areas, with dose-dependent effects in the cerebellum. Cytokine profiles (IL-1β, IL-6 and TNF-α) increased in a dose-dependent manner in different brain tissues. Exposure to 150 mg/kg of permethrin induced degenerated and/or dead neurons in the rat hippocampus and induced mitochondrial uncoupling and reduction of oxidative phosphorylation and significantly decreased the respiratory parameters state 3-associated respiration in complex I and II. PERM exposure at low doses induces reactive oxygen species production and imbalance in the enzymatic antioxidant system, increases gene expression of pro-inflammatory interleukins, and could lead to cell damage mediated by mitochondrial functional impairment. |
