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Titolo:
Inducible nitric oxide synthase knockout mice exhibit resistance to the multiple organ failure induced by zymosan
Autore:
Cuzzocrea, S; Mazzon, E; Dugo, L; Barbera, A; Centorrino, T; Ciccolo, A; Fonti, MT; Caputi, AP;
Indirizzi:
Univ Messina, Sch Med, Inst Pharmacol, I-98100 Messina, Italy Univ Messina Messina Italy I-98100 nst Pharmacol, I-98100 Messina, Italy Univ Messina, Sch Med, Dept Biomorphol, Messina, Italy Univ Messina Messina Italy na, Sch Med, Dept Biomorphol, Messina, Italy Univ Messina, Inst Gen Surg, Messina, Italy Univ Messina Messina ItalyUniv Messina, Inst Gen Surg, Messina, Italy
Titolo Testata:
SHOCK
fascicolo: 1, volume: 16, anno: 2001,
pagine: 51 - 58
SICI:
1073-2322(200107)16:1<51:INOSKM>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
CELLULAR-ENERGY DEPLETION; LIPID-PEROXIDATION; POLY(ADP-RIBOSE) SYNTHETASE; TYROSINE NITRATION; N-ACETYLCYSTEINE; ENDOTOXIC-SHOCK; LUNG INJURY; DNA-DAMAGE; PEROXYNITRITE; RAT;
Keywords:
iNOS; peroxynitrite; zymosan; free radicals; inflammation;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
54
Recensione:
Indirizzi per estratti:
Indirizzo: Cuzzocrea, S Univ Messina, Sch Med, Inst Pharmacol, Torre Biol,Policlin Univ Via C Valeria, I-98100 Messina, Italy Univ Messina Torre Biol,Policlin Univ Via C Valeria Messina Italy I-98100
Citazione:
S. Cuzzocrea et al., "Inducible nitric oxide synthase knockout mice exhibit resistance to the multiple organ failure induced by zymosan", SHOCK, 16(1), 2001, pp. 51-58

Abstract

In the present study, by comparing the responses in wild-type mice (+/+) and mice lacking (-/-) the inducible (or type 2) nitric oxide synthase (iNOS), we investigated the role played by iNOS in the development of non-septicshock. A severe inflammatory response characterized by peritoneal exudation, high peritoneal levels of nitrate/nitrite, and leukocyte infiltration into peritoneal exudate was induced by zymosan administration in iNOS +/+ mice. This inflammatory process coincided with the damage of lung, liver, and small intestine, as assessed by histological examination. Lung, small intestine, and liver myeloperoxidase (MPO) activity, indicative of neutrophil infiltration and lipid peroxidation, were significantly increased in zymosan-treated iNOS +/+ mice. Peritoneal administration of zymosan in the iNOS +/mice induced also a significant increase in the plasma levels of nitrite/nitrate and in the levels of peroxynitrite at 18 h after zymosan challenge. Immunohistochemical examination demonstrated a marked increase in the immunoreactivity to nitrotyrosine and to poly ADP-ribose synthetase (PARS) in the lung, liver, and intestine of zymosan-treated iNOS +/+ mice. The intensity and degree of nitrotyrosine and PARS were markedly reduced in tissue section from zymosan-iNOS -/- mice. Zymosan-treated iNOS -/- mice showed a significantly decreased mortality and inhibition of the development of peritonitis. In addition, iNOS -/- mice showed a significant protection on the development of organ failure since tissue injury and MPO were reduced in lung, small intestine, and liver. Furthermore, a significant reduction of suppression of mitochondrial respiration, DNA strand breakage, and reduction of cellular levels of NAD(+) was observed in ex vivo macrophages harvested from the peritoneal cavity of iNOS -/- mice subjected to zymosan-induced non-septic shock. in vivo treatment with aminoguanidine (300 mg/kg 1 and 6 h afterzymosan administration) significantly prevents the inflammatory process. Taken together, our results clearly demonstrate that iNOS plays an importantrole in zymosan-induced non-septic shock.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 03/06/20 alle ore 08:56:15