Abstract
Isolated rat liver mitochondria exposed to Fe(II)citrate undergo lipid peroxidation and alterations in membrane proteins. These processes were associated with irreversible decrease in membrane potential and mitochondrial swelling. Lipid peroxidation was evidenced by the production of thiobarbituric acid-reactive substances and also by the reaction of these products with membrane proteins, through the formation of Schiff bases. Alterations in membrane proteins were also characterized by the loss of specific proteins that could be recovered from the mitochondrial supernatant as shown by SDS-polyacrylamide gel electrophoresis. The degree of both lipid peroxidation and alterations in membrane proteins were diminished by EGTA, ruthenium red, or dibucaine. This strongly indicates that Ca2+ potentiates the oxidative damage of mitochondria exposed to Fe(II)citrate.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Calcium / metabolism
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Calcium / pharmacology*
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Citric Acid
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Drug Synergism
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Egtazic Acid / pharmacology
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Ferrous Compounds / toxicity*
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Intracellular Membranes / drug effects
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Intracellular Membranes / physiology
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Iron / pharmacology
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Kinetics
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Lipid Peroxidation / drug effects*
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Membrane Potentials / drug effects
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Membrane Proteins / drug effects
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Membrane Proteins / isolation & purification
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Membrane Proteins / metabolism*
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Mitochondria, Liver / drug effects*
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Mitochondria, Liver / metabolism
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Mitochondria, Liver / ultrastructure
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Mitochondrial Swelling / drug effects
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Onium Compounds / pharmacology
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Organophosphorus Compounds / pharmacology
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Oxygen Consumption / drug effects*
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Rats
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Rats, Wistar
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Ruthenium Red / pharmacology
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Time Factors
Substances
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Ferrous Compounds
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Membrane Proteins
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Onium Compounds
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Organophosphorus Compounds
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Ruthenium Red
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Citric Acid
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ferrous citrate
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Egtazic Acid
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Iron
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Calcium
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tetraphenylphosphonium