Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
LEUKOTOXIN (9,10-EPOXY-12-OCTADECENOATE) IMPAIRS ENERGY AND REDOX STATE OF ISOLATED-PERFUSED RAT LUNG
Autore:
AKAI M; ISHIZAKI T; MATSUKAWA S; SHIGEMORI K; MIYAMORI I;
Indirizzi:
FUKUI MED UNIV,FAC MED,DEPT INTERNAL MED 3 MATSUOKA FUKUI 91011 JAPAN FUKUI MED UNIV,FAC MED,CENT RES LABS MATSUOKA FUKUI 91011 JAPAN
Titolo Testata:
Free radical biology & medicine
fascicolo: 4-5, volume: 25, anno: 1998,
pagine: 596 - 604
SICI:
0891-5849(1998)25:4-5<596:L(IEAR>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
INDUCED OXIDATIVE STRESS; MUSCLE CELL CARDIOMYOCYTE; NITRIC-OXIDE; HYDROGEN-PEROXIDE; PULMONARY VASOCONSTRICTION; BIOSYNTHESIS; DYSFUNCTION; METABOLISM; INHIBITION; ACONITASE;
Keywords:
LEUKOTOXIN; ENDOTHELIN-1; ENERGY BALANCE; REDOX STATE; ANTIOXIDANT STATE; NITRIC OXIDE; SUPEROXIDE ANION; FREE RADICAL;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
30
Recensione:
Indirizzi per estratti:
Citazione:
M. Akai et al., "LEUKOTOXIN (9,10-EPOXY-12-OCTADECENOATE) IMPAIRS ENERGY AND REDOX STATE OF ISOLATED-PERFUSED RAT LUNG", Free radical biology & medicine, 25(4-5), 1998, pp. 596-604

Abstract

We investigated the perturbation of energy balance and redox state inleukotoxin (9, 10-epoxy-12-octadecenoate) (Lx)- and endothelin-1 (ET-1)-induced lung injury, using isolated perfused rat lungs. To examine any relationship between these parameters, intracellular levels of adenine nucleotides, pyridine coenzymes and glutathione were determined by reversed-phase high-performance liquid chromatography (HPLC) in the freeze-dried tissues of isolated rat lungs. The tissue samples were perfused with a physiological salt solution containing either Lx only, Lx plus N-G-monomethyl-L-arginine (L-NMMA), Lx plus N-G-monomethyl-D-arginine (D-NMMA), Lx plus superoxide dismutase (SOD) or ET-1 only. In isolated perfused lung tissue, 10 mu mol of Lx caused permeability-increased lung injury, and 10 nM of ET-1, which caused a comparable increase in wet lung weight, evoked pulmonary capillary hypertensive lung injury. Lx-injured lungs showed decreases in the contents of ATP, NADPH,NADH, reduced glutathione (GSH), (2ATP + ADP)/2(ATP + ADP + AMP) ratio (energy charge) and NADH/NAD(+) ratio, and increased the contents ofADP and AMP compared with the vehicle control and ET-1-injured lungs. Such effects of Lx were significantly attenuated by pretreatment with0.4 mM L-NMMA or 500 units/ml of SOD, but not with 0.4 mM D-NMMA. On the other hand, the ET-1-injured lung evidenced decreased tissue GSH. These findings indicate that Lx shifted the lung redox state toward oxidation and that Lx-induced lung injury was involved in the imbalance of the energy and redox state via production of nitric oxide and/or superoxide anion. (C) 1998 Elsevier Science Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/11/20 alle ore 08:39:15