Acute neurotoxic effects of paraquat on striatal mitochondrial function.

ANALÍA CZERNICZYNIEC; ESTELA LANZA; JUANITA BUSTAMANTE; SILVIA LORES-ARNAIZ

Valdivia

Congreso; VI Neurotoxicity Meeting: Mechanisms for neurodegenerative disorders.; 2013

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.