Journal of Bioenergetics and Biomembranes

, Volume 47, Issue 5, pp 395–408 | Cite as

Impairment of striatal mitochondrial function by acute paraquat poisoning

  • Analía Czerniczyniec
  • E. M. Lanza
  • A. G. Karadayian
  • J. Bustamante
  • S. Lores-Arnaiz


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. The aim of the present study was to evaluate changes in cortical and striatal mitochondrial function in an experimental model of acute paraquat toxicity and to compare if the brain areas and the molecular mechanisms involved were similar to those observed after chronic exposure. Sprague-Dawley rats received paraquat (25 mg/Kg i.p.) or saline and were sacrificed after 24 h. Paraquat treatment decreased complex I and IV activity by 37 and 21 % respectively in striatal mitochondria. Paraquat inhibited striatal state 4 and state 3 KCN-sensitive respiration by 80 % and 62 % respectively, indicating a direct effect on respiratory chain. An increase of 2.2 fold in state 4 and 2.3 fold in state 3 in KCN-insensitive respiration was 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 cardiolipin oxidation/depletion (12 %) in striatal mitochondria. Also, changes in mitochondrial polarization 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 induced a clear striatal mitochondrial dysfunction due to both paraquat redox cycling reactions and impairment of the mitochondrial electron transport, causing oxidative damage. As a consequence, mitochondrial dysfunction could probably lead to alterations in cellular bioenergetics.


Acute paraquat Mitochondrial function Oxygen consumption Membrane potential 



3, 3″-dihexyloxacarbocyanine iodide


ethylenediaminetetraacetic acid


carbonyl cyanide p-trifluoromethoxyphenylhydrazone


horseradish peroxidase


hydrogen peroxide


acridine orange 10-nonyl bromide


superoxide dismutase


thiobarbituric acid-reactive substances


Conflict of interest

The authors declare that there are no conflicts of interest.


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Copyright information

© Springer Science+Business Media New York 2015

Authors and Affiliations

  • Analía Czerniczyniec
    • 1
  • E. M. Lanza
    • 1
  • A. G. Karadayian
    • 1
  • J. Bustamante
    • 2
  • S. Lores-Arnaiz
    • 1
  1. 1.Instituto de Bioquímica y Medicina Molecular (UBA-CONICET), Facultad de Farmacia y BioquímicaUniversidad de Buenos AiresBuenos AiresArgentina
  2. 2.Centro de Altos Estudios en Ciencias Humanas y de la Salud (CAECIHS), Facultad de MedicinaUniversidad Abierta InteramericanaBuenos AiresArgentina

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