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Prior exercise protects against oxidative stress and motor deficit in a rat model of Parkinson’s disease

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Abstract

This study investigated if a prior long-term physical exercise protocol protects the substantia nigra and the striatum against oxidative stress and motor deficits in a Parkinson Disease model induced by 6-hydroxydopamine. Three animal treatment groups were included in the study: sham; 6-hydroxydopamine and 6-hydroxydopamine/exercise. Previously to the intrastriatal lesion by 6-hydroxydopamine, rats in the exercise groups performed a swimming program for 18 weeks. The rats were submitted to behavioral tests before and after intrastriatal 6-hydroxydopamine injection. The oxidative stress was analyzed by Thiobarbituric Acid Reactive Substances and Glutathione reductase activity methods. The exercise decreased lipid peroxidation and increased glutathione reductase activity in the substantia nigra. In contrast, in the striatum, exercise increased lipid peroxidation and decreased glutathione reductase activity. Exercise increased contralateral rotations and reduces immobility levels at 14 days post lesion. The exercise prior to 6-OHDA lesion had protective action only in substantia nigra against oxidative stress.

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Acknowledgements

To Elizabeth Sumi Yamada, Anderson Valente Amaral e Riky Douglas Gomes for helping the researchers with the manuscript translation.

Funding

This study was funded by Fundação Amazônia de Amparo a Estudos e Pesquisas (FAPESPA) by the technical cooperation agreement n° 003/2014-FAPESPA/UEPA.

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Correspondence to Leonam Oliver Durval Oliveira.

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All procedures performed in studies involving animals were in accordance with the ethical standards of the institution or practice at which the studies were conducted. (University of Pará State’s Ethics Committee - protocol number 39/14).

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The authors declare that they have no conflict of interest.

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Oliveira, L.O.D., da Silva, P.I.C., Filho, R.P.R. et al. Prior exercise protects against oxidative stress and motor deficit in a rat model of Parkinson’s disease. Metab Brain Dis 35, 175–181 (2020). https://doi.org/10.1007/s11011-019-00507-z

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  • DOI: https://doi.org/10.1007/s11011-019-00507-z

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