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  • Auranofin increases apoptosis and ischaemia-reperfusion injury in the rat isolated heart

    Author(s)
    Venardos, K
    Harrison, G
    Headrick, J
    Perkins, A
    Griffith University Author(s)
    Headrick, John P.
    Perkins, Anthony V.
    Harrison, Glenn J.
    Venardos, Kylie
    Year published
    2004
    Metadata
    Show full item record
    Abstract
    1. Auranofin, an antirheumatic gold compound, is an inhibitor of selenocysteine enzymes, such as thioredoxin reductase and glutathione peroxidase. These enzymes play an important role in protecting cardiac tissue from oxidative stress generated during ischaemia-reperfusion. 2. Auranofin (100 mg/kg) was administered to rats and their hearts were subjected to an in vitro model of ischaemia-reperfusion. The activity of thioredoxin reductase and glutathione peroxidase was determined in liver and heart tissues in an attempt to correlate enzymatic activity with heart recovery after ischaemia-reperfusion. 3. There was ...
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    1. Auranofin, an antirheumatic gold compound, is an inhibitor of selenocysteine enzymes, such as thioredoxin reductase and glutathione peroxidase. These enzymes play an important role in protecting cardiac tissue from oxidative stress generated during ischaemia-reperfusion. 2. Auranofin (100 mg/kg) was administered to rats and their hearts were subjected to an in vitro model of ischaemia-reperfusion. The activity of thioredoxin reductase and glutathione peroxidase was determined in liver and heart tissues in an attempt to correlate enzymatic activity with heart recovery after ischaemia-reperfusion. 3. There was significantly less thioredoxin reductase activity in rat liver extracts, whereas the level of glutathione activity remained unchanged, demonstrating that the dose of auranofin used was able to selectively inhibit one of these enzyme systems. Rats administered auranofin displayed significantly impaired recovery from ischaemic insult. The end diastolic pressure was increased, whereas the rate pressure product was significantly decreased. 4. The level of postischaemic apoptosis was also assessed by examining caspase-3 activity in tissue homogenates. Auranofin significantly increased the degree of postischaemic apoptosis, leading to poor postischaemic recovery.
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    Journal Title
    Clinical and Experimental Pharmacology and Physiology
    Volume
    31
    Issue
    5-6
    DOI
    https://doi.org/10.1111/j.1440-1681.2004.03993.x
    Copyright Statement
    © 2004 Blackwell Publishing. The definitive version is available at [www.blackwell-synergy.com.]
    Subject
    Zoology
    Pharmacology and pharmaceutical sciences
    Medical physiology
    History, heritage and archaeology
    Publication URI
    http://hdl.handle.net/10072/5662
    Collection
    • Journal articles

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