The amelioration of hepatocyte oxidative stress injury by nitric oxide released from S-nitroso-N-acetyl penicillamine: a study in immobilized perfused hepatocytes
Language English Country Spain Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
10445231
DOI
10.1358/mf.1999.21.6.541919
PII: 541919
Knihovny.cz E-resources
- MeSH
- Nitric Oxide Donors pharmacology MeSH
- Galactosamine toxicity MeSH
- Cells, Immobilized MeSH
- Liver cytology drug effects metabolism MeSH
- Rats MeSH
- Chemical and Drug Induced Liver Injury MeSH
- Liver Diseases drug therapy metabolism MeSH
- Nitric Oxide pharmacokinetics physiology MeSH
- Oxidative Stress drug effects MeSH
- Penicillamine analogs & derivatives pharmacokinetics pharmacology MeSH
- Perfusion MeSH
- Rats, Wistar MeSH
- tert-Butylhydroperoxide toxicity MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Nitric Oxide Donors MeSH
- Galactosamine MeSH
- Nitric Oxide MeSH
- Penicillamine MeSH
- S-nitro-N-acetylpenicillamine MeSH Browser
- tert-Butylhydroperoxide MeSH
S-nitroso-N-acetyl penicillamine (SNAP, 0.1-0.5 mM) caused release of nitric oxide (NO) into the perfusion medium of immobilized hepatocytes. Oxidative injury of hepatocytes was evoked by tert-butyl hydroperoxide (TBH, 1 mM) and the functional and morphological ultrastructural integrity of the cells was monitored. At the end of a 270-min perfusion period, SNAP-induced NO reduced lactate dehydrogenase leakage in TBH-injured hepatocytes as compared to untreated TBH-injured cells (122% +/- 5 vs. 146% +/- 6 of control levels), lipid peroxides production (2.7 +/- 0.2 vs. 3.7 +/- 0.3 nmol/10(6) cells), increased O2 consumption (26 +/- 2 vs. 12 +/- 1 nmol/10(6) cells) although urea synthesis was reduced. SNAP improved the formation of granules in the Golgi complex as compared to untreated TBH-injured hepatocytes and preserved the ultrastructural architecture of mitochondria and the smooth endoplasmic reticulum. The present data support a possible protective role of NO in oxidative liver injury.
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