Heparin-released extracellular superoxide dismutase is reduced in patients with coronary artery atherosclerosis

Tasaki, Hiromi; Yamashita, Kazuhito; Tsutsui, Masato; Kamezaki, Fumihiko; Kubara, Takahiro; Tanaka, Seiya; Sasaguri, Yasuyuki; Adachi, Tetsuo; Nakashima, Yasuhide

doi:10.1016/j.atherosclerosis.2005.08.028

Cited by 18 publications

(19 citation statements)

References 29 publications

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“…Ly s i s o f erythrocytes and epithelium develop following myocardial infarction (Simic et al 2003) allowing uncontrolled leakage of intracellular antioxidants into the blood stream and thus increasing the amounts of antioxidants found in peripheral blood sera. It is also likely that aspirin as well as heparin injection could influence antioxidant capacity in time points OV, I and II, although the most recent data (Tasaki et al 2006) suggest that heparin-released extracellular superoxide dismutase is significantly reduced in patients with coronary artery disease and that the tissue-bound location of this enzyme might be important for antioxidant function rather than its serum values. In case of heparin treatment and the tissue damage due to AMI and PCI treatment, heparin-released extracellular superoxide dismutase could be important parameter of the total serum antioxidant capacity.…”

Section: Discussionmentioning

confidence: 99%

Persistent Oxidative Stress after Myocardial Infarction Treated by Percutaneous Coronary Intervention

Nikolić-Heitzler

Rabuzin

Tatzber

et al. 2006

Tohoku J. Exp. Med.

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[247][248][249][250][251][252][253][254][255] Acute myocardial infarction causing cardiac ischemia is responsible for the majority of cardiac related deaths. Medical interventions that ensure rapid reperfusion, such as percutaneous coronary intervention, are aimed to allow myocardial re-oxygenation. However, this generates reactive oxygen species, resembling ischemiareperfusion type of injury based on oxidative stress. In the present study we monitored dynamic changes of total serum peroxides, total antioxidant capacity and soluble intercellular adhesion molecule-1 as well as the titer of antibodies against oxidized low-density lipoproteins in the blood during the convalescence period of 32 patients with acute myocardial infarction treated by percutaneous coronary intervention. Samples were taken at admittance and at two hours, four hours, three days and seven days following percutaneous coronary intervention. Total antioxidant capacity dropped to 82% ( p < 0.05). The titer of antibodies against oxidized low-density lipoproteins transiently decreased within the first three days, and increased afterwards. The values of serum peroxides and soluble intercellular adhesion molecule-1 increased continuously in respect to the initial levels reaching the maximum at the time of release from hospital. These findings indicate a persistent oxidative stress that might be associated with intravascular inflammation in patients during convalescence and release from hospital. myocardial infarction; percutaneous coronary intervention; inflammation; soluble intercellular adhesion molecule-1; lipid peroxidation © 2006 Tohoku University Medical Press While oxidative stress has been shown to be related with the age and living habits (Ozbay and Dulker 2002), it plays an important role in the development of vascular diseases that affect vital organs, in particular brain and heart (Zarkovic 2003;Zarkovic et al. 2004;Madamanchi et al.

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Section: Discussionmentioning

confidence: 99%

Persistent Oxidative Stress after Myocardial Infarction Treated by Percutaneous Coronary Intervention

Nikolić-Heitzler

Rabuzin

Tatzber

et al. 2006

Tohoku J. Exp. Med.

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“…Antioxidant effect of EC-SOD appears mainly on the vascular wall, not inside the volume of the bloodstream [10,17]. It was established that human coronary artery diseases are reliably connected with the decreased level of heparin-released EC-SOD [22,23]. Its positive correlation with the level of highdensity lipoprotein cholesterol and the age was noted [23].…”

Section: Extracellular Superoxide Dismutasementioning

confidence: 99%

“…It was established that human coronary artery diseases are reliably connected with the decreased level of heparin-released EC-SOD [22,23]. Its positive correlation with the level of highdensity lipoprotein cholesterol and the age was noted [23]. Protective effect of EC-SOD is explained by protection of vessel dilatator NO which is diffusing from the endothelium cells to guanylatcyclase of the smooth muscle cells [10,17,24].…”

Section: Extracellular Superoxide Dismutasementioning

confidence: 99%

“…The notable interest of researches to EC-SOD [16,17,[20][21][22][23][24][25][26][27][28] that is the (SOD-3) tetramer of Cu,Zn-SOD with high affinity to heparan sulphate [29][30][31] in the mammals, or its dimer form of Cu,Zn-SOD with low affinity to heparan sulphate [16,29,31] in the rats (as a result, the rats represent actually almost physiological knocked-out model for this enzyme) caused the development of gene therapy approaches aimed at ensuring antioxidant activity of the organism due to transfer of the appropriate genes [10,32]. Antioxidant gene therapy proved to be successful in experimental models of restenosis (rabbits, rats, pigs, etc.)…”

Section: Experimental Study Of Antioxidant Gene Therapymentioning

confidence: 99%

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Enzymatic Antioxidants: Next Phase of Pharmacological Effort to Fight Oxidative Stress?

Maksimenko¹,

Vavaev²,

Tischenko³

2010

TOPROCJ

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Abstract:The focus in the research of antioxidants is notably displaced in favour of research of enzyme derivatives. Extracellular superoxide dismutase (EC-SOD) is of the particular interest, as it demonstrates in vivo the protective action against development of atherosclerosis, hypertension, heart failure, diabetes mellitus. The reliable association of coronary artery disease with the decreased level of heparin-released EC-SOD was established in clinical researches. To base and develop antioxidant therapy, various SOD isozymes, catalase (CAT), the methods of experimental gene therapy, combined application of SOD-and CAT-activities are used. Covalent bienzyme SOD -CHS -CAT conjugate (where CHS -chondroitin sulphate) showed in the experimental trials its high efficacy as the antithrombotic agent. Pre-clinical research data approve the reliable option to gain for it the status of drug candidate. The trend to use the components of glycocalyx and extracellular matrix for target delivery of medical substances is evident. Development of new enzyme antioxidants for therapeutical destination is closely connected with becoming and progress of medical biotechnology, pharmaceutical industry, bioeconomy.

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“…As for factors affecting the level of heparin-induced ecSOD release, high-density lipoprotein cholesterol levels and age were correlated positively. 82 Because heparin is a common therapeutic drug for pulmonary embolism and deep vein thrombosis, an interesting question is whether heparin-induced ecSOD release also facilitates the therapeutic effect of heparin. …”

mentioning

confidence: 99%

Extracellular superoxide dismutase (ecSOD) in vascular biology: an update on exogenous gene transfer and endogenous regulators of ecSOD

Qin

Reszka

Fukai

et al. 2008

Translational Research

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Extracellular superoxide dismutase (ecSOD) is the major extracellular scavenger of superoxide () and a main regulator of nitric oxide (NO) bioactivity in the blood vessel wall, heart, lungs, kidney, and placenta. Involvement of has been implicated in many pathological processes, and removal of extracellular by ecSOD gene transfer has emerged as a promising experimental technique to treat vascular disorders associated with increased oxidant stress. In addition, recent studies have clarified mechanisms that regulate ecSOD expression, tissue binding, and activity, and they have provided new insight into how ecSOD interacts with other factors that regulate vascular function. Finally, studies of a common gene variant in humans associated with disruption of ecSOD tissue binding suggest that displacement of the enzyme from the blood vessel wall may contribute to vascular diseases. The purpose of this review is to summarize recent research findings related to ecSOD function and gene transfer and to stimulate other investigations into the role of this unique antioxidant enzyme in vascular pathophysiology and therapeutics.Oxidative stress induced by superoxide anion ( ) produced in vascular cells is involved in the pathogenesis of cardiovascular and metabolic diseases, including atherosclerosis, 1 ischemia-reperfusion injury, 2 diabetes, 3 hyperlipidemia, 4 and hypertension. 5 Moreover, may also contribute to pulmonary hypertension, 5 erectile dysfunction, 6 cerebral vasospasm, 7 and other disorders associated with vascular dysfunction. Consequently, strategies to reduce levels of have emerged as promising approaches to treating cardiovascular diseases and other conditions associated with enhanced oxidative stress. In mammalian tissues, 3 isoforms of SODs exist: Cu/Zn SOD (SOD1), Mn SOD (SOD2), and extracellular SOD (ecSOD or SOD3). SOD1 is an abundant copper-and zinc-containing cellular protein that is present in the cytosol, nucleus, peroxisomes, and mitochondrial inner membrane. Its primary function is to lower the intracellular steady-state concentration of . SOD1 mutations are associated with neural diseases such as amyotrophic lateral sclerosis. 8 SOD2 is a mitochondrial enzyme that disposes of generated by respiratory chain activity. SOD2 can be induced to protect against prooxidant insults. Conversely, SOD2 activity is decreased in physiologic aging and in diseases such as progeria, cancer, asthma, and transplant rejection. 9 ecSOD, another copper-and zinc-containing dismutase, is a primary antioxidant enzyme secreted to the extracellular space. ecSOD is expressed highly in selected tissues, including blood vessels, heart, lungs, kidney, placenta, and extracellular fluids. ecSOD plays an important role in regulating blood pressure and vascular contraction, at least in part, through modulating the endothelial function by controlling the levels of extracellular and nitric oxide bioactivity in the vasculature. 10,11 ecSOD has also been proposed to play an important role in neurologic, pulmonary, and arthriti...

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Heparin-released extracellular superoxide dismutase is reduced in patients with coronary artery atherosclerosis

Cited by 18 publications

References 29 publications

Persistent Oxidative Stress after Myocardial Infarction Treated by Percutaneous Coronary Intervention

Persistent Oxidative Stress after Myocardial Infarction Treated by Percutaneous Coronary Intervention

Enzymatic Antioxidants: Next Phase of Pharmacological Effort to Fight Oxidative Stress?

Extracellular superoxide dismutase (ecSOD) in vascular biology: an update on exogenous gene transfer and endogenous regulators of ecSOD

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