IBIMOL   23987
INSTITUTO DE BIOQUIMICA Y MEDICINA MOLECULAR PROFESOR ALBERTO BOVERIS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Evaluation of mitochondrial function in striatum and substantia nigra from atrazine-treated animals
Autor/es:
JUANITA BUSTAMANTE; ANALIA G. KARADAYIAN; ANALIA CZERNICZYNIEC; SILVIA LORES ARNAIZ
Lugar:
Buenos Aires
Reunión:
Congreso; 2nd FALAN Congress 2016; 2016
Institución organizadora:
Federation of Latinamerican Neuroscience Societies
Resumen:
Atrazine (ATZ) is a widely used herbicidedescribed as a potential environmental neurotoxin. As mitochondrial dysfunction has been linkedwithneurodegenerative diseases, the aim of this work was to evaluate the effect of sub-chronic administration of ATZ on mitochondrial function from cerebral cortex, striatum and substantia nigra. SD rats received ATZ(5 mg/Kg i.p.),3 times a week during a month. Results: State 4 oxygen consumption was increased by 60 and 74 % and state 3 oxygen consumption was decreased by 27% and 55% in striatal and nigral mitochondria from treated animals respectively. In addition, respiratory control decreased after ATZ treatment. Atrazine induced a decrease in complex I activity by 20% in both brain areas and inhibitedcomplex IV activity by 32% in striatum. Evaluation of hydrogen peroxide production by striatal and nigral mitochondria from treated animals showed an increase of 26 and 96 % respectively. Also, ATZ treatment induced mitochondrial depolarization in striatal mitochondriabut had non-significant effects on substantia nigra.No significant changes were observed after ATZ treatment in any of the mitochondrial parameters evaluated in cortical mitochondria.This work showed that sub-chronic exposure to ATZ induces striatal and nigral mitochondrial dysfunction modifying cellular bioenergetics that could lead to neuronal death. Furthermore,substantia nigra would be more susceptible to ATZ-damage than striatum and cerebral cortex.