Evaluation of mitochondrial function in striatum and substantia nigra from atrazine-treated animals.

CZERNICZYNIEC, A.; KARADAYIAN, A.; BUSTAMANTE, J.;; LORES-ARNAIZ, S.

Buenos Aires

Congreso; 2nd Federation of Latinamerican Neuroscience Societies (FALAN) Congress 2016; 2016

Sociedad Argentina de Investigación en Neurociencias - Federation of Latin American and Caribbean Neuroscience Societies

Atrazine (ATZ) is a widely used herbicide described as a potential environmental neurotoxin associated with neurodegenerative disorders. As mitochondrial dysfunction has been linked with neurodegenerative 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 O2 consumption was increased by 60 and 74 % and state 3 O2 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 inhibited complex 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 mitochondria but 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.