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Paper Information

Title: 

NECROTIC CELL DEATH DUE TO REDUCTIVE STRESS INDUCED BY MITOCHONDRIAL RESPIRATORY INHIBITORS

Type: SPEECH
Author(s): NIKNAHAD H.*
 
 *DEPARTMENT OF PHARMACOLOGY AND TOXICOLOGY, FACULTY OF PHARMACY, SHIRAZ UNIVERSITY OF MEDICAL SCIENCES, SHIRAZ, FARS, IRAN, 71345-1583
 
Name of Seminar: IRANIAN CONGRESS OF TOXICOLOGY
Type of Seminar:  CONGRESS
Sponsor:  SOCIETY OF TOXICOLOGY
Date:  2004Volume 8
 
 
Abstract: 

Hypoxia or chemical hypoxia, induced by mitochondrial respiratory inhibitors, results in necrotic cell death in different organs including the liver it is commonly believed that hypoxia or chemical hypoxia results in cell death by depleting cellular ATP level. However, the results of this study suggest that cytotoxicity induced by the mitochondrial respiratory inhibitors or hypoxia: reoxygenation injury could be attributed not only to ATP depletion but also to reductive stress and oxygen activation. Hypoxia, cyanide or antimycin A markedly depletes hepatocyte ATP level and increases reductive stress, non-heme Fe release and H2O2 formation in hepatocytes. Cytotoxicity was partly prevented by the ferric chelator desferoxamine, the xanthine oxidase inhibitor oxypurinol and the hydrogen peroxide scavenger glutathione. No lipid peroxidation could be detected and phenolic antioxidants had little effect. Increasing the NADH/NAD+ ratio with NADH generating compounds markedly increased cytotoxicity and the intracellular free Fe. On the other hand, NADH utilizing substrates, which decrease the reductive stress, prevented cytotoxicity and Fe release. The results suggest that liver injury resulting from insufficient respiration involves reductive stress which releases intracellular Fe, converts xanthine dehydrogenase to xanthine oxidase and causes mitochondrial oxygen activation.

 
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