Title of article :
Intermittent Anoxia Reduces Oxygen Free Radicals Formation During Reoxygenation in Rat Hepatocytes
Author/Authors :
Antonio Gasbarrini، نويسنده , , Alessandra Colantoni، نويسنده , , Cristiana Di Campli، نويسنده , , Stefania De Notariis، نويسنده , , Michele Masetti، نويسنده , , Elio Iovine، نويسنده , , Alighieri Mazziotti، نويسنده , , Irene Massari، نويسنده , , Giovanni Gasbarrini and on behalf of the Alcoholism Treatment Study Group، نويسنده , , Paolo Pola، نويسنده , , Mauro Bernardi، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 1997
Pages :
6
From page :
1067
To page :
1072
Abstract :
The sensitivity of liver cells to anoxia is a major problem afflicting liver preservation and transplantation. Intermittent ischemia has been proposed to reduce reperfusion injury. The aim of the study was to assess oxygen free radical formation and cell injury during continuous or intermittent anoxia/reoxygenation in rat hepatocytes. Anion superoxide was measured by lucigenin-enhanced chemiluminescence and cell damage by LDH release and trypan blue uptake. During anoxia, superoxide generation dropped to background level in both groups; trypan blue uptake and LDH release, which increased progressively, were significantly greater in hepatocytes exposed to continuous compared to intermittent anoxia. During reoxygenation, a massive generation of superoxide anion formation, followed by a sharp increase in LDH release, was observed in both groups. However, both oxyradical generation and cell injury were significantly greater in cells exposed to continuous compared to intermittent anoxia. The data, showing that intermittent oxygen deprivation reduce liver cell injury and oxygen free radical formation determined by anoxia/reoxygenation, suggest a novel possible approach to the reduction of reperfusion injury.
Keywords :
hepatocytes , Anoxia , Reoxygenation , oxygen free radicals , Cell injury
Journal title :
Free Radical Biology and Medicine
Serial Year :
1997
Journal title :
Free Radical Biology and Medicine
Record number :
517723
Link To Document :
بازگشت