Antioxidants Sample Clauses

Antioxidants. Redox status is a term which describes the balance between free radical generation and antioxidant capacity. Antioxidants are molecules which detoxify oxidants, such as free radicals, and prevent the oxidation of other molecules73. They are therefore essential in protecting the heart from ROS induced injury. Superoxide dismutase (SOD), catalyses the dismutation of ∙O - to H O , which in turn is decomposed to water and oxygen by catalase. α-tocopherol (Vitamin E) reacts with peroxyl radicals to yield a stable tocopheroxyl radical which is recycled back to α-tocopherol by ascorbate. Ascorbate also scavenges ∙O -, ∙HO2 and ∙OH59. Glutathione peroxidise (GSH-Px) uses reduced glutathione (GSH) as a substrate to decompose peroxides (including lipid peroxides and H2O2) to form water and oxidised glutathione (GSSG). GSH itself is an antioxidant which has a strong tendency to donate electrons and is capable of reducing other molecules directly, therefore is capable of recycling other oxidised antioxidants, for example, ascorbate. Numerous studies have demonstrated the importance of the antioxidant system in protecting the heart from ROS induced injury. For example, mice over expressing SOD subjected to ischaemia for 35 minutes displayed decreases in myocardial infarction size post ischaemia compared to wild type mice74. SOD knockout mice display more myocardial hypertrophy in response to ischaemia induced myocardial infarction compared to wild type mice75. Upon reperfusion, SOD administration improved myocardial contractile function in ischaemic- reperfused rabbit hearts compared to control hearts76. GSH administration also improved myocardial contractile dysfunction on the reperfusion of ischaemic isolated rat hearts77. Ascorbate and α-tocopherol have also been implicated in the protection against ischaemia induced myocardial injury78,79. These studies emphasise the importance of ROS generation and altered redox status in myocardial dysfunction. To summarise, hypoxia and ROS generation, and changes in cellular redox status as a result of myocardial ischaemia can eventually cause irreversible cell injury, leading to necrosis and myocardial infarction. Identification of hypoxic myocardium and/or altered myocardial redox status may therefore provide an opportunity to diagnose vulnerable tissue and intervene before ischaemic injury becomes irreversible.
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Antioxidants. Do they have a place in the prevention or therapy of acute kidney injury? Nephron Exp Nephrol 2008; 109: e109-117.
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