Mitochondrial calcium, oxidative stress and apoptosis in a neurodegenerative disease model induced by 3-nitropropionic acid

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dc.contributor.author Rosenstock, Tatiana Rosado [UNIFESP]
dc.contributor.author Carvalho, Ana Carolina Pereira de [UNIFESP]
dc.contributor.author Jurkiewicz, Aron [UNIFESP]
dc.contributor.author Frussa-Filho, Roberto [UNIFESP]
dc.contributor.author Smaili, Soraya Soubhi [UNIFESP]
dc.date.accessioned 2016-01-24T12:34:18Z
dc.date.available 2016-01-24T12:34:18Z
dc.date.issued 2004-03-01
dc.identifier http://dx.doi.org/10.1046/j.1471-4159.2003.02250.x
dc.identifier.citation Journal of Neurochemistry. Oxford: Blackwell Publishing Ltd, v. 88, n. 5, p. 1220-1228, 2004.
dc.identifier.issn 0022-3042
dc.identifier.uri http://repositorio.unifesp.br/handle/11600/27635
dc.description.abstract Intracellular calcium homeostasis is important for cell survival. However, increase in mitochondrial calcium (Ca-m(2+)) induces opening of permeability transition pore (PTP), mitochondrial dysfunction and apoptosis. Since alterations of intracellular Ca2+ and reactive oxygen species (ROS) generation are involved in cell death, they might be involved in neurodegenerative processes such as Huntington's disease (HD). HD is characterized by the inhibition of complex II of respiratory chain and increase in ROS production. in this report, we studied the correlation between the inhibitor of the complex II, 3-nitropropionic acid (3NP), Ca2+ metabolism, apoptosis and behavioural alterations. We showed that 3NP (1 mM) is able to release Ca-m(2+), as neither Thapsigargin (TAP, 2 muM) nor free-calcium medium affected its effect. PTP inhibitors and antioxidants inhibited this process, suggesting an increase in ROS generation and PTP opening. in addition, 3NP (0.1 mM) also induces apoptotic cell death. Behavioural changes in animals treated with 3NP (20 mg/kg/day for 4 days) were also attenuated by pre- and co-treatment with vitamin E (VE, 20 mg/kg/day). Taken together, our results show that complex II inhibition could involve Ca-m(2+) release, oxidative stress and cell death that may precede motor alterations in neurodegenerative processes such as HD. en
dc.format.extent 1220-1228
dc.language.iso eng
dc.publisher Blackwell Publishing Ltd
dc.relation.ispartof Journal of Neurochemistry
dc.rights Acesso aberto
dc.subject apoptosis en
dc.subject calcium en
dc.subject Huntington's disease en
dc.subject mitochondria en
dc.subject neurodegeneration en
dc.subject 3-nitropropionic acid en
dc.title Mitochondrial calcium, oxidative stress and apoptosis in a neurodegenerative disease model induced by 3-nitropropionic acid en
dc.type Artigo
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.description.affiliation Universidade Federal de São Paulo, Dept Farmacol, UNIFESP EPM, BR-04044020 São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Dept Farmacol, UNIFESP EPM, BR-04044020 São Paulo, Brazil
dc.identifier.doi 10.1046/j.1471-4159.2003.02250.x
dc.description.source Web of Science
dc.identifier.wos WOS:000189051800019



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