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Titolo:
Formation of 4-hydroxy-2-nonenal-modified proteins in ischemic rat heart
Autore:
Eaton, P; Li, JM; Hearse, DJ; Shattock, MJ;
Indirizzi:
St Thomas Hosp, Rayne Inst, London SE1 7EH, England St Thomas Hosp London England SE1 7EH ayne Inst, London SE1 7EH, England
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
fascicolo: 3, volume: 45, anno: 1999,
pagine: H935 - H943
SICI:
0363-6135(199903)45:3<H935:FO4PII>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
FREE-RADICAL GENERATION; DEPLETION IMPAIRS RECOVERY; NA+-K+-ATPASE; MYOCARDIAL GLUTATHIONE; LIPID-PEROXIDATION; POSTISCHEMIC REPERFUSION; VENTRICULAR MYOCYTES; S-CONJUGATE; PROTECTION; PRODUCT;
Keywords:
oxidant stress; free radical; lipid peroxidation; reperfusion;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
46
Recensione:
Indirizzi per estratti:
Indirizzo: Eaton, P St Thomas Hosp, Rayne Inst, London SE1 7EH, England St Thomas Hosp London England SE1 7EH , London SE1 7EH, England
Citazione:
P. Eaton et al., "Formation of 4-hydroxy-2-nonenal-modified proteins in ischemic rat heart", AM J P-HEAR, 45(3), 1999, pp. H935-H943

Abstract

Hydroxy-2-nonenal (HNE) is a major lipid peroxidation product formed during oxidative stress. Because of its reactivity with nucleophilic compounds, particularly metabolites and proteins containing thiol groups, HNE is cytotoxic. The aim of this study was to assess the extent and time course for the formation of HNE-modified proteins during ischemia and ischemia plus reperfusion in isolated rat hearts. With an antibody to HNE-Cys/His/Lys and densitometry of Western blots, we quantified the amount of HNE-protein adduct in the heart. By taking biopsies from single hearts (n = 5) at various times (0, 5, 10, 15, 20, 35, and 40 min) after onset of zero-flow global ischemia, we showed a progressive, time-dependent increase (which peaked after 30min) in HNE-mediated modification of a discrete number of proteins. In studies with individual hearts (n = 4/group), control aerobic perfusion (70 min) resulted in a very low level (296 arbitrary units) of HNE-protein adductformation; by contrast, after 30-min ischemia HNE-adduct content increasedby >50-fold (15,356 units, P < 0.05). In other studies (n = 4/group), administration of N-(2-mercaptopropionyl)glycine (MPG, 1 mM) to the heart for 5min immediately before 30-min ischemia reduced HNE-protein adduct formation during ischemia by similar to 75%. In studies (n = 4/group) that includedreperfusion of hearts after 5, 10, 15, or 30 min of ischemia, there was nofurther increase in the extent of HNE-protein adduct formation over that seen with ischemia alone. Similarly, in experiments with MPG, reperfusion did not significantly influence the tissue content of HNE-protein adduct. Western immunoblot results were confirmed in studies using in situ immunofluorescent localization of HNE-protein in cryosections. In conclusion, ischemiacauses a major increase in HNE-protein adduct that would be expected to reflect a toxic sequence of events that might act to compromise tissue survival during ischemia and recovery on reperfusion.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 08/07/20 alle ore 01:40:11