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Evaluation of purine nucleotide loss, lipid peroxidation and ultrastructural alterations in post‐hypoxic hepatocytes.
Author(s) -
Grune T,
Müller K,
Zöllner S,
Haseloff R,
Blasig I E,
David H,
Siems W
Publication year - 1997
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1997.sp021877
Subject(s) - glutathione , lipid peroxidation , chemistry , oxidative stress , biochemistry , thiobarbituric acid , radical , mitochondrion , cell damage , enzyme
1. Hypoxic alterations in isolated rat hepatocytes were demonstrated by a 90% ATP loss during 60 min of ischaemia and temporary increases of nucleotide degradation products. 2. The oxidative stress during reoxygenation was demonstrated in these cells by a decrease in reduced glutathione (GSH) concentration (30%) and a threefold increase in lipid peroxidation products such as 4‐hydroxynonenal and thiobarbituric acid‐reactive substances (TBA‐RSs). The tremendous GSH loss could not be balanced by the slight oxidized glutathione (GSSG) increase during reoxygenation. 3. For the first time the involvement of free radicals was directly demonstrated using electron spin resonance (ESR) spectroscopy in reoxygenated liver cells. Using the spin trap 5,5‐dimethylpyrroline‐1‐oxide (DMPO), a carbon‐centred radical and the adduct of the hydroxyl radical could be detected during early reoxygenation. 4. Morphological alteration of cells was observed, beginning during hypoxia and increasing during post‐hypoxic reoxygenation. Electron microscopic findings of hypoxic and post‐hypoxic cell damage included pyknosis of nuclei, spherical transformation of mitochondria and increased number of vesicles.