IBIMOL   23987
INSTITUTO DE BIOQUIMICA Y MEDICINA MOLECULAR PROFESOR ALBERTO BOVERIS
Unidad Ejecutora - UE
artículos
Título:
Impairment of striatal mitochondrial function by acute paraquat poisoning
Autor/es:
ANALIA CZERNICZYNIEC; ESTELA LANZA; ANALIA G. KARADAYIAN; JUANITA BUSTAMANTE; SILVIA LORES ARNAIZ
Revista:
JOURNAL OF BIOENERGETICS AND BIOMEMBRANES
Editorial:
SPRINGER/PLENUM PUBLISHERS
Referencias:
Lugar: New York; Año: 2015 vol. 47 p. 395 - 408
ISSN:
0145-479X
Resumen:
Mitochondria are essential for survival. Their primaryfunction is to support aerobic respiration and to provideenergy for intracellular metabolic pathways. Paraquat is a redoxcycling agent capable of generating reactive oxygen species.The aim of the present study was to evaluate changes incortical and striatal mitochondrial function in an experimentalmodel of acute paraquat toxicity and to compare if the brainareas and the molecular mechanisms involved were similar tothose observed after chronic exposure. Sprague-Dawley ratsreceived paraquat (25 mg/Kg i.p.) or saline and weresacrificed after 24 h. Paraquat treatment decreased complex Iand IVactivity by 37 and 21 % respectively in striatal mitochondria.Paraquat inhibited striatal state 4 and state 3 KCNsensitiverespiration by 80%and 62%respectively, indicatinga direct effect on respiratory chain. An increase of 2.2 fold instate 4 and 2.3 fold in state 3 in KCN-insensitive respirationwas observed in striatal mitochondria from paraquat animals,suggesting that paraquat redox cycling also consumed oxygen.Paraquat treatment increased hydrogen peroxide production(150 %), TBARS production (42 %) and cardiolipinoxidation/depletion (12 %) in striatal mitochondria. Also,changes in mitochondrial polarization was induced after paraquattreatment. However, no changes were observed in any ofthese parameters in cortical mitochondria from paraquattreated-animals. These results suggest that paraquat treatmentinduced a clear striatal mitochondrial dysfunction due to bothparaquat redox cycling reactions and impairment of the mitochondrialelectron transport, causing oxidative damage. As aconsequence, mitochondrial dysfunction could probably leadto alterations in cellular bioenergetics.