http://www.cnr.it/ontology/cnr/individuo/prodotto/ID184390

Redox Proteomics in Aging Rat Brain: Involvement of Mitochondrial Reduced Glutathione Status and Mitochondrial Protein Oxidation in the Aging Process (Articolo in rivista)

Type

Articolo in rivista (Classe)
Prodotto della ricerca (Classe)

Label

Redox Proteomics in Aging Rat Brain: Involvement of Mitochondrial Reduced Glutathione Status and Mitochondrial Protein Oxidation in the Aging Process (Articolo in rivista) (literal)

Anno

2010-01-01T00:00:00+01:00 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi

10.1002/jnr.22500 (literal)

Alternative label

Perluigi, M (Perluigi, M.)1; Di Domenico, F (Di Domenico, F.)1; Giorgi, A (Giorgi, A.)1; Schinina, ME (Schinina, M. E.)1; Coccia, R (Coccia, R.)1; Cini, C (Cini, C.)1; Bellia, F (Bellia, F.)2; Cambria, MT (Cambria, M. T.)2; Cornelius, C (Cornelius, C.)2; Butterfield, DA (Butterfield, D. A.)3,4; Calabrese, V (Calabrese, V.)2,5 (2010)
Redox Proteomics in Aging Rat Brain: Involvement of Mitochondrial Reduced Glutathione Status and Mitochondrial Protein Oxidation in the Aging Process
in Journal of neuroscience research; WILEY-LISS, DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 (Stati Uniti d'America)
(literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori

Perluigi, M (Perluigi, M.)1; Di Domenico, F (Di Domenico, F.)1; Giorgi, A (Giorgi, A.)1; Schinina, ME (Schinina, M. E.)1; Coccia, R (Coccia, R.)1; Cini, C (Cini, C.)1; Bellia, F (Bellia, F.)2; Cambria, MT (Cambria, M. T.)2; Cornelius, C (Cornelius, C.)2; Butterfield, DA (Butterfield, D. A.)3,4; Calabrese, V (Calabrese, V.)2,5 (literal)

Pagina inizio

3498 (literal)

Pagina fine

3507 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume

88 (literal)

Rivista

Journal of neuroscience research (Rivista)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#pagineTotali

10 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo

16 (literal)

Note

ISI Web of Science (WOS) (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni

1. Univ Roma La Sapienza, Dept Biochem Sci, I-00185 Rome, Italy 2. Univ Catania, Dept Chem Sci, Catania, Italy 3. Univ Kentucky, Ctr Membrane Sci, Dept Chem, Lexington, KY 40506 USA 4. Univ Kentucky, Sanders Brown Ctr Aging, Lexington, KY 40536 USA 5. Natl Inst Biosyst & Biostruct, Catania Sect, Catania, Italy (literal)

Titolo

Redox Proteomics in Aging Rat Brain: Involvement of Mitochondrial Reduced Glutathione Status and Mitochondrial Protein Oxidation in the Aging Process (literal)

Abstract

Increasing evidence supports the notion that increased oxidative stress is a fundamental cause in the aging process and in neurodegenerative diseases. As a result, a decline in cognitive function is generally associated with brain aging. Reactive oxygen species (ROS) are highly reactive intermediates, which can modify proteins, nucleic acids, and polyunsaturated fatty acids, leading to neuronal damage. Because proteins are major components of biological systems and play key roles in a variety of cellular functions, oxidative damage to proteins represents a primary event observed in aging and age-related neurodegenerative disorders. In the present study, with a redox proteomics approach, we identified mitochondrial oxidatively modified proteins as a function of brain aging, specifically in those brain regions, such as cortex and hippocampus, that are commonly affected by the aging process. In all brain regions examined, many of the identified proteins were energy-related, such as pyruvate kinase, ATP synthase, aldolase, creatine kinase, and alpha-enolase. These alterations were associated with significant changes in both cytosolic and mitochondrial redox status in all brain regions analyzed. Our finding is in line with current literature postulating that free radical damage and decreased energy production are characteristic hallmarks of the aging process. In additon, our results further contribute to identifying common pathological pathways involved both in aging and in neurodegenerative disease development. (literal)

Editore