Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
OXIDATIVE-METABOLISM IN RAT HEPATOCYTES AND MITOCHONDRIA DURING SEPSIS
Autore:
KANTROW SP; TAYLOR DE; CARRAWAY MS; PIANTADOSI CA;
Indirizzi:
DUKE UNIV,MED CTR,DEPT MED,BOX 3315 DURHAM NC 27710 DUKE UNIV,MED CTR,DEPT ANESTHESIOL DURHAM NC 27710 UNIV TEXAS,MED CTR,DEPT MED HOUSTON TX 77030
Titolo Testata:
Archives of biochemistry and biophysics
fascicolo: 2, volume: 345, anno: 1997,
pagine: 278 - 288
SICI:
0003-9861(1997)345:2<278:OIRHAM>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; DENSITY GRADIENT CENTRIFUGATION; BLUE NATIVE ELECTROPHORESIS; ENDOGENOUS NITRIC-OXIDE; LIVER-MITOCHONDRIA; ULTRASTRUCTURAL-CHANGES; CYTOCHROME-OXIDASE; RESPIRATORY-CHAIN; PROTEIN OXIDATION; FACTOR-ALPHA;
Keywords:
SEPSIS; HEPATOCYTE; MITOCHONDRIA; RESPIRATION; OXIDATIVE STRESS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
53
Recensione:
Indirizzi per estratti:
Citazione:
S.P. Kantrow et al., "OXIDATIVE-METABOLISM IN RAT HEPATOCYTES AND MITOCHONDRIA DURING SEPSIS", Archives of biochemistry and biophysics, 345(2), 1997, pp. 278-288

Abstract

We hypothesized that cellular oxygen consumption is abnormal during sepsis as a result of increased oxidative stress and selective mitochondrial damage, In a rat model of sepsis (cecal ligation and puncture), we studied the respiratory characteristics of isolated hepatocytes andliver mitochondria 16 h after onset of septic injury. Endogenous respiration by isolated cells was decreased during sepsis, while cyanide-resistant (nonmitochondrial) respiration was unaffected. Maximal oxygenconsumption in ADP-supplemented, permeabilized hepatocytes was decreased with succinate as the substrate, but not with malate + glutamate or TMPD + ascorbate, In contrast, maximum oxygen consumption (State 3) by isolated liver mitochondria increased up to 35% during sepsis usingeither succinate or malate + glutamate as substrate, The electrophoretic features and mobility of nondenatured mitochondrial respiratory complexes were similar in control and septic hepatocytes, with the exception of decreased Complex V protein in sepsis. Structural evaluation of mitochondria in fixed liver slices by electron microscopy showed mitochondrial swelling in most of the septic animals. Measurements of oxidative stress during sepsis suggested an increase in hydroxylation of salicylate by isolated hepatocytes, and mitochondrial protein carbonylcontent was increased significantly. Induction of iNOS in hepatocytesafter 16 h of sepsis was variable, and little release of the oxidation products of NO . was detected. These findings are interpreted to mean that hepatocytes contain a mixed population of injured and hyperfunctional mitochondria during sepsis. (C) 1997 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/07/20 alle ore 19:58:25