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Titolo:
Superoxide dismutase and pulmonary oxygen toxicity: Lessons from transgenic and knockout mice (Review)
Autore:
Tsan, MF;
Indirizzi:
Stratton Dept Vet Affairs Med Ctr, Res Serv, Albany, NY 12208 USA StrattonDept Vet Affairs Med Ctr Albany NY USA 12208 lbany, NY 12208 USA Albany Med Coll, Ctr Cardiovasc Biol, Albany, NY 12208 USA Albany Med Coll Albany NY USA 12208 Cardiovasc Biol, Albany, NY 12208 USA
Titolo Testata:
INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
fascicolo: 1, volume: 7, anno: 2001,
pagine: 13 - 19
SICI:
1107-3756(200101)7:1<13:SDAPOT>2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
ANTIOXIDANT DEFENSE-MECHANISMS; TUMOR-NECROSIS-FACTOR; LUNG INJURY; HYDROGEN-PEROXIDE; PROTECTS RATS; TRACHEAL INSUFFLATION; RADICAL PRODUCTION; ELEVATED LEVELS; DEFICIENT MICE; DOWNS-SYNDROME;
Keywords:
superoxide dismutase; knockout mice; pulmonary oxygen toxicity;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
78
Recensione:
Indirizzi per estratti:
Indirizzo: Tsan, MF Stratton Dept Vet Affairs Med Ctr, Res Serv, Albany, NY 12208 USAStratton Dept Vet Affairs Med Ctr Albany NY USA 12208 12208 USA
Citazione:
M.F. Tsan, "Superoxide dismutase and pulmonary oxygen toxicity: Lessons from transgenic and knockout mice (Review)", INT J MOL M, 7(1), 2001, pp. 13-19

Abstract

Superoxide (O-2(-)) has been implicated in the pathogenesis of pulmonary O-2 toxicity. The studies using transgenic and knockout mice of each of the three isoforms of superoxide dismutase (SOD) e.g., CuZnSOD, MnSOD and extracellular SOD (EC-SOD), have demonstrated that O-2(-) produced in the mitochondria from its electron transport system and extracellular O-2(-) generated by infiltrating neutrophils, and possibly its derivatives e.g., hydroxyl radical and peroxynitrite, are important mediators of hyperoxia-induced pulmonary injury, while cytoplasmic O-2(-) plays a limited, if any, role in the pathogenesis of pulmonary O-2 toxicity. Distal airway epithelial cells including type II alveolar and non-ciliated bronchiolar epithelial cells, areimportant targets for O-2 radicals under the hyperoxic condition. The accessibility of these distal airway epithelial cells to in vivo gene transfer through the tracheal route of administration, suggests the potential for invivo transfer of MnSOD and EC-SOD genes as a future approach in the prevention of pulmonary O-2 toxicity.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/11/20 alle ore 22:50:20