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Titolo:
Extracellular superoxide dismutase attenuates lung injury after hemorrhage
Autore:
Bowler, RP; Arcaroli, J; Crapo, JD; Ross, A; Slot, JW; Abraham, E;
Indirizzi:
Natl Jewish Med & Res Ctr, Denver, CO 80206 USA Natl Jewish Med & Res CtrDenver CO USA 80206 s Ctr, Denver, CO 80206 USA Univ Colorado, Hlth Sci Ctr, Div Pulm Sci & Crit Care Med, Denver, CO USA Univ Colorado Denver CO USA Div Pulm Sci & Crit Care Med, Denver, CO USA Univ Utrecht, Dept Pathol, Utrecht, Netherlands Univ Utrecht Utrecht Netherlands cht, Dept Pathol, Utrecht, Netherlands
Titolo Testata:
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
fascicolo: 2, volume: 164, anno: 2001,
pagine: 290 - 294
SICI:
1073-449X(20010715)164:2<290:ESDALI>2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
RESPIRATORY-DISTRESS SYNDROME; HUMAN ENDOTHELIAL-CELLS; NF-KAPPA-B; NEUTROPHIL ACTIVATION; SELECTIN EXPRESSION; PROTEIN-KINASE; FREE-RADICALS; SHOCK; ENDOTOXEMIA; MECHANISMS;
Keywords:
hemorrhage; extracellular superoxide dismutase; NF-kappa B; myeloperoxidase;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
41
Recensione:
Indirizzi per estratti:
Indirizzo: Bowler, RP Natl Jewish Med & Res Ctr, K707,1400 Jackson St, Denver, CO 80206 USA Natl Jewish Med & Res Ctr K707,1400 Jackson St Denver CO USA 80206
Citazione:
R.P. Bowler et al., "Extracellular superoxide dismutase attenuates lung injury after hemorrhage", AM J R CRIT, 164(2), 2001, pp. 290-294

Abstract

Reperfusion of the lung after hemorrhage generates free radicals such as superoxide (O-2') that may injure the lung; however, the relative importanceof intracellular versus extracellular free radicals is unclear. The superoxide dismutases (SOD) are the primary enzymatic method to reduce superoxide. We examined whether lung-specific overexpression of extracellular superoxide dismutase (EC-SOD) would attenuate hemorrhage-induced lung injury. Wildtype mice and mice overexpressing the human EC-SOD gene with a lung-specific promoter were hemorrhaged by removing 30% of blood volume. After hemorrhage, the lung wet to dry weight ratios increased from 5.4 +/- 0.11 in unmanipulated control mice to 6.3 +/- 0.16 in wild-type mice, but to only 5.60 +/- 0.17 in the EC-SOD transgenic mice (p < 0.05 compared with hemorrhaged wildtype). Hemorrhage-induced lipid peroxidation, as assessed by lung F-2 isoprostanes, was lower in the EC-SOD transgenic mice (3.4 +/- 0.3 mug/lung) compared with wild-type mice (1.9 +/- 0.2 mug/lung; p < 0.05). Compared withwild-type, EC-SOD transgenic mice had attenuated the hemorrhage-induced increase in both pulmonary nuclear factor kappa B (NK-kappaB) activation (relative absorbance 1.1 +/- 0.2 for EC-SOD transgenic versus 2.5 +/- 0.1 for wild-type; p < 0.05) and myeloperoxidase activity (5.1 +/- 0.87 units/g for EC-SOD transgenic versus 11.3 +/- 1.8 units/g for wild-type; p < 0.01). Thus, overexpression of pulmonary EC-SOD in the mouse lung attenuates lung injury after hemorrhage.

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Documento generato il 04/04/20 alle ore 15:12:44