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Acta Cir Bras ; 20 Suppl 1: 72-7, 2005.
Article in English | MEDLINE | ID: mdl-16186974

ABSTRACT

PURPOSE: The aim of this work was to investigate the hypothesis that catechol inhibits FADH -linked basal respiration in mitochondria isolated from rat liver homogenates. Moreover, catechol ability to induce peroxidation of biomolecules in liver nuclear fractions was also studied. METHODS: Rat liver homogenates were incubated with 1mM 1,2-dihydroxybenzene (catechol) at pH 7.4 for up to 30 minutes. After that, mitochondrial fractions were isolated by differential centrifugation. Basal oxygen uptake was measured using a Clark-type electrode after the addition of 10 mM sodium succinate. Nuclear fractions were incubated in the presence of 1 mM catechol for 17 hours at room temperature and the peroxidation of biomolecules was investigated by the reaction with thiobarbituric acid, which was determined spectrophotometrically at 535 nm. RESULTS: Catechol induced a time-dependent partial inhibition of FADH -linked basal mitochondrial respiration, however this substance was unable to induce a direct peroxidation of biomolecules in hepatic nuclear fractions. CONCLUSION: Catechol produced an inhibition of basal respiration associated to FADH2 in isolated liver mitochondria that could lead to cytotoxicity, ROS generation and cell death.


Subject(s)
Catechols/toxicity , Flavin-Adenine Dinucleotide/analogs & derivatives , Lipid Peroxidation/drug effects , Mitochondria, Liver/drug effects , Oxidative Stress/drug effects , Oxygen Consumption/drug effects , Animals , Cell Nucleus/drug effects , Cell Respiration/drug effects , Enzyme Inhibitors/pharmacology , Flavin-Adenine Dinucleotide/antagonists & inhibitors , Mitochondria, Liver/metabolism , Rats , Rats, Wistar , Reactive Oxygen Species/metabolism , Time Factors
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