2013
DOI: 10.5152/akd.2013.186
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The effect of antioxidant enzyme levels and exercise on syndrome X and coronary slow flow phenomenon: an observational study

Abstract: Objective: In this study the antioxidant enzyme [catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) ] levels at rest in patients with syndrome X and coronary slow flow are measured. Then it has been investigated whether there is any enzymatic difference between the normal controls and syndrome X patients or patients with coronary slow flow and ascertain if exercise has any effects on the antioxidant enzyme levels. Methods: Fifty-five patients were included in this prospective observat… Show more

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Cited by 5 publications
(5 citation statements)
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References 21 publications
(25 reference statements)
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“…Oster et al ( 31 ) reported that cardiac output correlates positively with cardiac Cu in patients with CHD. Erythrocyte superoxide dismutase was decreased in patients examined 6 months after myocardial infarction ( 32 ) and in patients with coronary slow flow ( 33 ) . Cu/Zn superoxide dismutase protects against oxidative damage and depends on Cu for activity ( 34 ) .…”
Section: The Copper Deficiency Theorymentioning
confidence: 99%
“…Oster et al ( 31 ) reported that cardiac output correlates positively with cardiac Cu in patients with CHD. Erythrocyte superoxide dismutase was decreased in patients examined 6 months after myocardial infarction ( 32 ) and in patients with coronary slow flow ( 33 ) . Cu/Zn superoxide dismutase protects against oxidative damage and depends on Cu for activity ( 34 ) .…”
Section: The Copper Deficiency Theorymentioning
confidence: 99%
“…No single underlying mechanism has been identified for the condition. Small vessel coronary artery disease, abnormal coronary vascular resistance, and subendocardial ischemia have been invoked as possible mechanisms, although none of these factors is universally accepted ( 3 , 4 ). Several studies have found abnormalities consistent with myocardial perfusion in patients with CSX using positron emission tomography ( 5 ), scintigraphic myocardial perfusion imaging ( 6 ), and nuclear magnetic resonance imaging ( 7 ).…”
Section: Introductionmentioning
confidence: 99%
“…The Nrf-2-antioxidant response element (AR E) signaling pathway regulates the encoding of antioxidant proteins through various interactions, and it is the central regulator of cellular antioxidant responses (33). The ARE, which is a cis-acting enhancer sequence of many antioxidant enzyme/protein gene upstream, is one of the defense mechanisms which enables the body to deal with oxidative stress (34). Previous findings have shown that Nrf-2 adjusts the encoding of antioxidant genes by interacting with ARE.…”
Section: Discussionmentioning
confidence: 99%
“…Previous findings have shown that Nrf-2 adjusts the encoding of antioxidant genes by interacting with ARE. Under normal conditions, Nrf-2 is localized in the cytoplasm, combined with the cytoplasmic protein Keap1; when subjected to attack from ROS, Nrf-2 dissociates from Keap1, translocates into the nucleus, binds to Maf protein in order to form a heterodimer, which binds to ARE in the gene to activate targeted gene expression as well as to regulate antioxidant enzyme/protein transcription (34,35). Thus, Nrf-2 is a receptor for oxidative stress, which plays an important role in the protection of cells against oxidative stress and it is one of the principal defense mechanisms induced by exposure to exogenous toxic substances (19).…”
Section: Discussionmentioning
confidence: 99%