The amelioration of hepatocyte oxidative stress injury by nitric oxide released from S-nitroso-N-acetyl penicillamine: a study in immobilized perfused hepatocytes
Jazyk angličtina Země Španělsko Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
10445231
DOI
10.1358/mf.1999.21.6.541919
PII: 541919
Knihovny.cz E-zdroje
- MeSH
- donory oxidu dusnatého farmakologie MeSH
- galaktosamin toxicita MeSH
- imobilizované buňky MeSH
- játra cytologie účinky léků metabolismus MeSH
- krysa rodu Rattus MeSH
- lékové postižení jater MeSH
- nemoci jater farmakoterapie metabolismus MeSH
- oxid dusnatý farmakokinetika fyziologie MeSH
- oxidační stres účinky léků MeSH
- penicilamin analogy a deriváty farmakokinetika farmakologie MeSH
- perfuze MeSH
- potkani Wistar MeSH
- terc-butylhydroperoxid toxicita MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- donory oxidu dusnatého MeSH
- galaktosamin MeSH
- oxid dusnatý MeSH
- penicilamin MeSH
- S-nitro-N-acetylpenicillamine MeSH Prohlížeč
- terc-butylhydroperoxid 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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