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  • Myocardial Antioxidant Enzyme Systems, Ischemia-Reperfusion Injury, and Selenium

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    Venardos_2005_01Thesis.pdf (2.740Mb)
    Author(s)
    Venardos, Kylie
    Primary Supervisor
    Perkins, Tony
    Other Supervisors
    Harrison, Glenn
    Headrick, John
    Year published
    2005
    Metadata
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    Abstract
    Coronary heart disease remains the greatest killer of Australian's, and given our ageing population, along with increasing risk factors, it is predicted to become an even more significant problem worldwide over the next 20 years. Reperfusion, without doubt is the most effective treatment for ischemic myocardium. However, this produces deleterious effects upon cells, and depending on the severity, may ultimately lead to cell death. While the pathogenesis of ischemia-reperfusion is not completely understood, there is considerable evidence implicating reactive oxygen species (ROS) as an initial cause of the injury. ROS formed ...
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    Coronary heart disease remains the greatest killer of Australian's, and given our ageing population, along with increasing risk factors, it is predicted to become an even more significant problem worldwide over the next 20 years. Reperfusion, without doubt is the most effective treatment for ischemic myocardium. However, this produces deleterious effects upon cells, and depending on the severity, may ultimately lead to cell death. While the pathogenesis of ischemia-reperfusion is not completely understood, there is considerable evidence implicating reactive oxygen species (ROS) as an initial cause of the injury. ROS formed during oxidative stress can initiate lipid peroxidation, oxidize proteins to inactive states and cause DNA strand breaks, all potentially damaging to normal cellular function. ROS have been shown to be generated following routine clinical procedures such as coronary bypass surgery and thrombolysis, due to the unavoidable episode of ischemiareperfusion. Furthermore, they have been associated with poor cardiac recovery post-ischemia, with recent studies supporting a role for them in infarction, necrosis, apoptosis, arrhythmogenesis and endothelial dysfunction following ischemia-reperfusion. In normal physiological condition, ROS production is usually homeostatically controlled by endogenous free radical scavengers such as SOD, catalase, and the glutathione peroxidase and thioredoxin reductase systems. Targeting the generation of ROS with various antioxidants has been shown to reduce injury following oxidative stress, and improve recovery from ischemia-reperfusion injury. This thesis investigates the role of myocardial antioxidant enzymes in ischemiareperfusion injury, particularly the glutathione peroxidase (GPX) and the thioredoxin reductase (TxnRed) systems. GPX and TxnRed are selenocysteine dependent enzymes, and their activity is known to be dependent upon an adequate supply of dietary selenium and selenocysteine. In mammalian cells, the generation of selenocysteine occurs during amino acid biosynthesis and the degree of selenium (Se) incorporation into the cysteine residue is concentration dependent. Previous studies have found that up-regulation of these systems is cardioprotective and down-regulation is detrimental following ischemia-reperfusion. This thesis attempts to extend these observations by increasing not only our understanding of the roles of myocardial antioxidant enzymes in ischemia-reperfusion injury, but also the effect of dietary selenium on these systems. Furthermore, it investigates the effects of ischemia, reperfusion, and ageing on myocardial antioxidant enzymes.
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    Thesis Type
    Thesis (PhD Doctorate)
    Degree Program
    Doctor of Philosophy (PhD)
    School
    School of Health Sciences
    DOI
    https://doi.org/10.25904/1912/3596
    Copyright Statement
    The author owns the copyright in this thesis, unless stated otherwise.
    Item Access Status
    Public
    Subject
    Coronary heart disease
    myocardial antoxidant
    ischemic myocardium
    reactive oxygen species
    ischemia-reperfusion injury
    selenium
    Publication URI
    http://hdl.handle.net/10072/365301
    Collection
    • Theses - Higher Degree by Research

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