Critical O2 and NO concentrations in NO-induced cell death in a rat liver sinusoidalendothelial cell line

Verfasser / Beitragende:
[N. Dehne, T. Li, F. Petrat, U. Rauen, H. de Groot]
Ort, Verlag, Jahr:
2004
Enthalten in:
Biological Chemistry, 385/3-4(2004-04-13), 341-349
Format:
Artikel (online)
ID: 378920030
LEADER caa a22 4500
001 378920030
003 CHVBK
005 20180305123603.0
007 cr unu---uuuuu
008 161128e20040413xx s 000 0 eng
024 7 0 |a 10.1515/BC.2004.030  |2 doi 
035 |a (NATIONALLICENCE)gruyter-10.1515/BC.2004.030 
245 0 0 |a Critical O2 and NO concentrations in NO-induced cell death in a rat liver sinusoidalendothelial cell line  |h [Elektronische Daten]  |c [N. Dehne, T. Li, F. Petrat, U. Rauen, H. de Groot] 
520 3 |a Nitric oxide (NO) plus oxygen (O2) are known to cause cell damage via formation of reactive nitrogen species. NO itself directly inhibits cytochrome oxidase of the mitochondrial respiratory chain in competition with O2, thus inducing a hypoxic-like injury. To assess the critical NO and O2 concentrations for both mechanisms of NO-induced cell injury, cells of a rat liver sinusoidal endothelial cell line were incubated in the presence of the NO donor spermineNONOate at different O2 concentrations, and their loss of viability was determined by the release of lactate dehydrogenase. Protection by ascorbic acid was used as indication for the involvement of reactive nitrogen species, whereas a hypoxiclike injury was indicated by the protective effects of glycine and glucose and the increase in NAD(P)H fluorescence. High concentrations of NO (approx. 10 uM NO) and O2 (21% O2) were required to induce endothelial cell death mediated by formation of reactive nitrogen species. On the other hand, pathophysiologically relevant NO concentrations at low but physiological O2 concentrations (ca. 2 uM NO at 5% O2 and about 1 uM NO at 2% O2) induced hypoxiclike cell death in the endothelial cells that was prevented by the presence of glucose. 
540 |a Copyright © 2004 by Walter de Gruyter GmbH & Co. KG 
690 7 |a Biochemistry  |2 nationallicence 
690 7 |a Molecular biology  |2 nationallicence 
690 7 |a Cellular biology  |2 nationallicence 
700 1 |a Dehne  |D N.  |4 aut 
700 1 |a Li  |D T.  |4 aut 
700 1 |a Petrat  |D F.  |4 aut 
700 1 |a Rauen  |D U.  |4 aut 
700 1 |a Groot  |D H. de  |4 aut 
773 0 |t Biological Chemistry  |d Walter de Gruyter  |g 385/3-4(2004-04-13), 341-349  |x 1431-6730  |q 385:3-4<341  |1 2004  |2 385  |o bchm 
856 4 0 |u https://doi.org/10.1515/BC.2004.030  |q text/html  |z Onlinezugriff via DOI 
908 |D 1  |a research article  |2 jats 
950 |B NATIONALLICENCE  |P 856  |E 40  |u https://doi.org/10.1515/BC.2004.030  |q text/html  |z Onlinezugriff via DOI 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Dehne  |D N.  |4 aut 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Li  |D T.  |4 aut 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Petrat  |D F.  |4 aut 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Rauen  |D U.  |4 aut 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Groot  |D H. de  |4 aut 
950 |B NATIONALLICENCE  |P 773  |E 0-  |t Biological Chemistry  |d Walter de Gruyter  |g 385/3-4(2004-04-13), 341-349  |x 1431-6730  |q 385:3-4<341  |1 2004  |2 385  |o bchm 
900 7 |b CC0  |u http://creativecommons.org/publicdomain/zero/1.0  |2 nationallicence 
898 |a BK010053  |b XK010053  |c XK010000 
949 |B NATIONALLICENCE  |F NATIONALLICENCE  |b NL-gruyter