Nitric Oxide Suppresses Hepatocyte Apoptosis Induced by Free Radicals.
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Accession number;01A0901048
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| Title;Nitric Oxide Suppresses Hepatocyte Apoptosis Induced by Free Radicals. |
| Author;
KISHIKAWA H
(Nippon Medical School, Tokyo, Jpn)
SAKAMOTO A
(Nippon Medical School, Tokyo, Jpn)
OGAWA R
(Nippon Medical School, Tokyo, Jpn)
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Journal Title;Biomed Res
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Journal Code:Z0236B
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ISSN:0388-6107
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VOL.22;NO.2;PAGE.83-89(2001)
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| Figure&Table&Reference;FIG.6, REF.27 |
| Pub. Country;Japan |
| Language;English |
| Abstract;When liver failure is induced by ischemia-reperfusion injury or sepsis, neutrophils or Kupffer cells produce reactive oxygen species (ROS), nitric oxide (NO), or peroxynitrite (ONOO-). These substances have been shown to induce cytotoxicity and apoptosis in various cells. In this study, using rat hepatocytes exposed to AAPH (free radical generator), NOC 18 (NO donor), and SIN-1 (peroxynitrite generator), we investigated which substance induced the earliest and most severe hepatocellular damage and apoptosis. Hepatocytes treated with 15 mM AAPH for 6 h showed significantly reduced viability, significantly increased apoptosis, and a significant increase of hepatocellular enzymes compared with control cells or with those exposed to 1mM NOC 18 and 1mM SIN-1. On the other hand, hepatocytes treated with a combination of 0.25mM NOC 18 and 15mM AAPH showed significantly increased cell viability, significantly reduced apoptosis, and significantly lower levels of hepatocellular enzymes compared with cells exposed to 15mM AAPH alone. These results indicate that free radicals may play a role in inducing hepatocyte damage and apoptosis in the early phase of acute liver failure, while low concentrations of NO have a cytoprotective effect against hepatocyte damage by free radicals. (author abst.) |
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