Ornithine In Vivo Administration Disrupts Redox Homeostasis and Decreases Synaptic Na+, K+-ATPase Activity in Cerebellum of Adolescent Rats: Implications for the Pathogenesis of Hyperornithinemia-Hyperammonemia-Homocitrullinuria (HHH) Syndrome-Reference-Cited by-同舟云学术

Ornithine In Vivo Administration Disrupts Redox Homeostasis and Decreases Synaptic Na+, K+-ATPase Activity in Cerebellum of Adolescent Rats: Implications for the Pathogenesis of Hyperornithinemia-Hyperammonemia-Homocitrullinuria (HHH) Syndrome

Published:2015-03-13 Issue:6 Volume:35 Page:797-806
ISSN:0272-4340
Container-title:Cellular and Molecular Neurobiology
language:en
Short-container-title:Cell Mol Neurobiol

Author:

Zanatta Ângela,Viegas Carolina Maso,Hickmann Fernanda Hermes,de Oliveira Monteiro Wagner,Sitta Angela,de Moura Coelho Daniela,Vargas Carmen Regla,Leipnitz Guilhian,Wajner Moacir

Publisher

Springer Science and Business Media LLC

Subject

Cell Biology,Cellular and Molecular Neuroscience,General Medicine

Link

http://link.springer.com/content/pdf/10.1007/s10571-015-0173-y.pdf

Reference74 articles.

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3. Amaral AU, Leipnitz G, Fernandes CG, Seminotti B, Zanatta A, Viegas CM, Dutra-Filho CS, Wajner M (2009) Evidence that the major metabolites accumulating in hyperornithinemia-hyperammonemia-homocitrullinuria syndrome induce oxidative stress in brain of young rats. Int J Dev Neurosci 7:635–641. doi: 10.1016/j.ijdevneu.2009.08.004

4. Amaral AU, Seminotti B, Cecatto C, Fernandes CG, Busanello EN, Zanatta Â, Kist LW, Bogo MR, de Souza DO, Woontner M, Goodman S, Koeller DM, Wajner M (2012) Reduction of Na+, K+-ATPase activity and expression in cerebral cortex of glutaryl-CoA dehydrogenase deficient mice: a possible mechanism for brain injury in glutaric aciduria type I. Mol Genet Metab 107:375–382. doi: 10.1016/j.ymgme.2012.08.016

5. Bagh MB, Maiti AK, Jana S, Banerjee K, Roy A, Chakrabarti S (2008) Quinone and oxyradical scavenging properties of N-acetylcysteine prevent dopamine mediated inhibition of Na+, K+-ATPase and mitochondrial electron transport chain activity in rat brain: implications in the neuroprotective therapy of Parkinson’s disease. Free Radic Res 42:574–581. doi: 10.1080/10715760802158430

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