Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2006-2-7
pubmed:abstractText
Mice that lack the mitochondrial form of superoxide dismutase (SOD2) incur severe pathologies and mitochondrial deficiencies, including major depletion of complex II, as a consequence of buildup of endogenous reactive oxygen species (Melov, S., Coskun, P., Patel, M., Tuinstra, R., Cottrell, B., Jun, A. S., Zastawny, T. H., Dizdaroglu, M., Goodman, S. I., Huang, T. T., Miziorko, H., Epstein, C. J., and Wallace, D. C. (1999) Proc. Natl. Acad. Sci. U. S. A. 96, 846-851 and Li, Y., Huang, T. T., Carlson, E. J., Melov, S., Ursell, P. C., Olson, J. L., Noble, L. J., Yoshimura, M. P., Berger, C., Chan, P. H., Wallace, D. C., and Epstein, C. J. (1995) Nat. Genet. 11, 376-381). These problems can be greatly attenuated or rescued by synthetic antioxidant treatment, such as with the catalytic antioxidant EUK189 (Hinerfeld, D., Traini, M. D., Weinberger, R. P., Cochran, B., Doctrow, S. R., Harry, J., and Melov, S. (2004) J. Neurochem. 88, 657-667). We have used heart mitochondria from sod2 null mice to better understand mitochondrial reactive oxygen species production both in the absence of SOD2 and following in vivo antioxidant treatment. Isolated heart mitochondria from 5-day-old sod2 null animals respiring on the complex II substrate succinate exhibited statistically significant higher levels of mitochondrial O2* (157%, p < 0.01) but significantly less H2O2 (33%, p < 0.001) than wild type littermates. Treatment of sod2 nullizygous mice with EUK189 proportionately increased the levels of complex II and H2O2. Increased production of O2* resulting from complex II normalization had no effect on steady state levels due to the rapid conversion to H2O2, a process presumably aided by the presence of the EUK189, an SOD mimetic.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Antioxidants, http://linkedlifedata.com/resource/pubmed/chemical/EUK-189, http://linkedlifedata.com/resource/pubmed/chemical/Ethidium, http://linkedlifedata.com/resource/pubmed/chemical/Hydrogen Peroxide, http://linkedlifedata.com/resource/pubmed/chemical/Organometallic Compounds, http://linkedlifedata.com/resource/pubmed/chemical/Oxazines, http://linkedlifedata.com/resource/pubmed/chemical/Oxygen, http://linkedlifedata.com/resource/pubmed/chemical/Reactive Oxygen Species, http://linkedlifedata.com/resource/pubmed/chemical/Salicylates, http://linkedlifedata.com/resource/pubmed/chemical/Superoxide Dismutase, http://linkedlifedata.com/resource/pubmed/chemical/Superoxides, http://linkedlifedata.com/resource/pubmed/chemical/amplex red reagent, http://linkedlifedata.com/resource/pubmed/chemical/dihydroethidium, http://linkedlifedata.com/resource/pubmed/chemical/superoxide dismutase 2
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
10
pubmed:volume
281
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3354-9
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:16326710-Animals, pubmed-meshheading:16326710-Antioxidants, pubmed-meshheading:16326710-Catalysis, pubmed-meshheading:16326710-Ethidium, pubmed-meshheading:16326710-Genotype, pubmed-meshheading:16326710-Hydrogen Peroxide, pubmed-meshheading:16326710-Immunoblotting, pubmed-meshheading:16326710-Mice, pubmed-meshheading:16326710-Mice, Transgenic, pubmed-meshheading:16326710-Mitochondria, pubmed-meshheading:16326710-Mitochondria, Heart, pubmed-meshheading:16326710-Organometallic Compounds, pubmed-meshheading:16326710-Oxazines, pubmed-meshheading:16326710-Oxidative Stress, pubmed-meshheading:16326710-Oxygen, pubmed-meshheading:16326710-Reactive Oxygen Species, pubmed-meshheading:16326710-Salicylates, pubmed-meshheading:16326710-Submitochondrial Particles, pubmed-meshheading:16326710-Superoxide Dismutase, pubmed-meshheading:16326710-Superoxides
pubmed:year
2006
pubmed:articleTitle
Mitochondrial reactive oxygen species in mice lacking superoxide dismutase 2: attenuation via antioxidant treatment.
pubmed:affiliation
Buck Institute for Age Research, Novato, California 94945, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural