INVESTIGADORES
LORES ARNAIZ Silvia
congresos y reuniones científicas
Título:
Acute neurotoxic effects of paraquat on striatal mitochondrial function.
Autor/es:
CZERNICZYNIEC, A.; LANZA, EM; BUSTAMANTE, J.; LORES ARNAIZ, S.
Lugar:
Valdivia
Reunión:
Congreso; VI Neurotoxicity Meeting: Mechanisms for neurodegenerative disorders.; 2013
Institución organizadora:
Neurotoxicity Society
Resumen:
Mitochondria are essential
for survival. Their primary function is to support aerobic respiration and to
provide energy for intracellular metabolic pathways. Paraquat is a redox
cycling agent capable of generating reactive oxygen species and oxidative
stress. The aim of this work was to evaluate the effect of acute intoxication
of paraquat on cortical and striatal mitochondrial function. SD female rats
received paraquat (25 mg/Kg
i.p.) or saline and were sacrificed after 1 hour. Paraquat treatment significantly
decreased complex I and IV activity by 30 and 17 % respectively in striatal mitochondria. State 4 oxygen
consumption was increased by 32 % and no changes were observed in state 3 oxygen
consumption in striatal mitochondria from treated-animals. Respiratory states 3 and
4 were not inhibited by cyanide. Paraquat treatment increased hydrogen peroxide production by 115% in striatal
mitochondria. Mitochondrial hyperpolarization was induced after paraquat
treatment However, no changes were observed in
any of these parameters in cortical mitochondria from paraquat treated animals.
These results
suggest that paraquat treatment disrupt striatal
mitochondrial function through an increment in reactive oxygen species, due to
its redox cycling metabolism and respiratory chain inhibition. As a
consequence, mitochondrial dysfunction could probably lead to alterations in cellular bioenergetics and neuronal
death.