000			02638na a2200253 4500
999			_c1843 _d1843
003			PC1843
005			20210625062757.0
008			130622s2013 xxx||||| |||| 00| 0 eng d
040			_cH12O
041			_aeng
100			_aBautista, José M. _91902 _eInstituto de Investigación i+12
100			_aDíez, Amalia _91901 _eInstituto de Investigación i+12
100			_aLinares Gómez, María _91898 _eInstituto de Investigación i+12
100			_aMarín García, Patricia _92240 _eInstituto de Investigación i+12
100			_aPuyet, Antonio _91900 _eInstituto de Investigación i+12
245	0	0	_aGlutathione peroxidase contributes with heme oxygenase-1 to redox balance in mouse brain during the course of cerebral malaria. _h[artículo]
260			_bBiochimica et biophysica acta. Molecular basis of disease, _c2013
300			_a1832(12):2009-18.
500			_aFormato Vancouver: Linares M, Marín-García P, Martínez-Chacón G, Pérez-Benavente S, Puyet A, Diez A et al. Glutathione peroxidase contributes with heme oxygenase-1 to redox balance in mouse brain during the course of cerebral malaria. Biochim Biophys Acta. 2013 Dec;1832(12):2009-18.
501			_aPMID: 23872112
504			_aContiene 50 referencias
520			_aOxidative stress has been attributed both a key pathogenic and rescuing role in cerebral malaria (CM). In a Plasmodium berghei ANKA murine model of CM, host redox signaling and functioning were examined during the course of neurological damage. Host antioxidant defenses were early altered at the transcriptional level indicated by the gradually diminished expression of superoxide dismutase-1 (sod-1), sod-2, sod-3 and catalase genes. During severe disease, this led to the dysfunctional activity of superoxide dismutase and catalase enzymes in damaged brain regions. Vitagene associated markers (heat shock protein 70 and thioredoxin-1) also showed a decaying expression pattern that paralleled reduced expression of the transcription factors Parkinson disease 7, Forkhead box 0 3 and X-box binding protein 1 with a role in preserving brain redox status. However, the oxidative stress markers reactive oxygen/nitrogen species were not accumulated in the brains of CM mice and redox proteomics and immunohistochemistry failed to detect quantitative or qualitative differences in protein carbonylation. Thus, the loss of antioxidant capacity was compensated for in all cerebral regions by progressive upregulation of heme oxygenase-1, and in specific regions by early glutathione peroxidase-1 induction. This study shows for the first time a scenario of cooperative glutathione peroxidase and heme oxygenase-1 upregulation to suppress superoxide dismutase, catalase, heat shock protein-70 and thioredoxin-1 downregulation effects in experimental CM, counteracting oxidative damage and maintaining redox equilibrium. Our findings reconcile the apparent inconsistency between the lack of oxidative metabolite build up and reported protective effect of antioxidant therapy against CM.
710			_9625 _aInstituto de Investigación imas12
856			_uhttp://pc-h12o-es.m-hdoct.a17.csinet.es/pdf/pc/1/pc1843.pdf _ySolicitar documento
942			_n0 _2ddc _cART