Hepatic damage induced by perfusion of radical generating azo compound and its inhibition by vitamin E

The damaging effect of perfusion of hydrophilic radical generating azo compound on the liver of normal and vitamin E-deficient rats and its inhibition by antioxidants were studied in order to increase understanding of the action of free radicals on biological tissues. The hepatic damage was evaluate...

Full description

Saved in:
Bibliographic Details
Published in:Chemico-biological interactions 1995-06, Vol.97 (1), p.11-23
Main Authors: Yasuda, Hiroshi, Noguchi, Noriko, Miki, Masayuki, Morinobu, Wakaba, Hirano, Kazuya, Ogihara, Thoru, Tanabe, Takuya, Mino, Makoto, Terao, Kiyoshi, Niki, Etsuo
Format: Article
Language:English
Subjects:
Active oxygen
Alanine Transaminase - blood
Amidines - pharmacology
Animals
Antioxidants
Aspartate Aminotransferases - blood
Azo Compounds - antagonists & inhibitors
Azo Compounds - toxicity
Biological and medical sciences
Chemical and Drug Induced Liver Injury - etiology
Chemical and industrial products toxicology. Toxic occupational diseases
Electron Spin Resonance Spectroscopy
Free radicals
Free Radicals - toxicity
Liver damage
Male
Medical sciences
Mitochondria, Liver - drug effects
Mitochondria, Liver - metabolism
Oxidative Phosphorylation - drug effects
Rats
Rats, Wistar
Toxicology
Various organic compounds
Vitamin E - pharmacology
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The damaging effect of perfusion of hydrophilic radical generating azo compound on the liver of normal and vitamin E-deficient rats and its inhibition by antioxidants were studied in order to increase understanding of the action of free radicals on biological tissues. The hepatic damage was evaluated from the release of cytosolic enzymes such as glutamic oxaloacetic transaminase and glutamic pyruvic transaminase, mitochondrial oxidation metabolism and morphological change. Two kinds of hydrophilic azo compounds were used, one which decomposes spontaneously at a uniform rate to generate free radicals and the other which does not. The former induced hepatic damage in a dose-dependent manner, while the latter did not exert any damage. Both endogenous vitamin E in the membranes and a watersoluble vitamin E analogue added simultaneously with a radical initiator suppressed the hepatic damage. These results show that the hepatic damage induced by perfusion of radical generating azo compound is caused not by the azo compound itself but by free radicals.
ISSN:0009-2797
1872-7786
DOI:10.1016/0009-2797(94)03604-5