Role of Cytokines, Tyrosine Kinase, and Protein Kinase C on Production of Superoxide and Induction of Scavenging Enzymes in Human Leukocytes

Niwa, Yukie; Ozaki, Yoshisuke; Kanoh, Tadashi; Akamatsu, Hirohiko; Kurisaka, Masahiro

doi:10.1006/clin.1996.0083

Cited by 58 publications

(44 citation statements)

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“…17 This is in concordance with other reports of a role for protein kinases in the regulation of induction of Mn-SOD in endothelial cells, 41,42 human lung adenocarcinoma cells, 43 and human leukocytes. 44 On the other hand, an important role has been demonstrated for ROS, cytokines, and nuclear factor-B, an oxidant-sensitive transcription factor, in modulating Mn-SOD gene expression, 18,22,[45][46][47] all of which have also been implicated in mediating delayed cardioprotective effects after ischemic preconditioning. 6,18,40,48 -50 The interaction between the transient activation of A 1 R and potential generation of ROS or the activation of cytokines or nuclear factor-B was not addressed in the present study and warrants further investigation.…”

Section: Cardioprotective Role Of Mn-sodmentioning

confidence: 99%

Adenosine A ₁ Receptor Activation Induces Delayed Preconditioning in Rats Mediated by Manganese Superoxide Dismutase

et al. 2000

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Background-We have previously described a second window of protection against infarction in rabbits 24 to 72 hours after adenosine A 1 receptor (A 1 R) activation. In this study, we examined the potential role of the mitochondrial antioxidant manganese superoxide dismutase (Mn-SOD) as a potential end effector in mediating this protection. Methods and Results-Rats were treated with an intravenous bolus of the A 1 R agonist 2-chloro-N 6 -cyclopentyladenosine (CCPA, 75 g/kg) or saline vehicle. They were also given a 5 mg/kg IV infusion of a 22-mer phosphorothioate oligodeoxynucleotide (ODN) with sequence antisense to the initiation site of rat Mn-SOD mRNA. Sense ODN and scrambled ODN were used as controls. Twenty-four hours later, hearts were isolated and perfused with buffer at constant pressure and subjected to 35 minutes of regional ischemia and 2 hours of reperfusion. Treatment with CCPA compared with saline vehicle (control) significantly reduced infarct size, expressed as percentage of myocardium at risk (22.3Ϯ3.3% versus 42.1Ϯ3.8%, respectively; Pϭ0.001). This protection was completely abolished by prior treatment with antisense ODN, which had no effect on its own. Neither sense ODN nor scrambled ODN had an effect on the CCPA-induced delayed cardioprotection. In separate animals, 24 hours after the same treatment, hearts were assayed for Mn-SOD content and activity. CCPA treatment induced a significant increase in myocardial Mn-SOD content and activity compared with the control condition; this increase was abolished by pretreatment with antisense ODN. Conclusions-This is the first study to show that transient A 1 R activation induces delayed cardioprotection in the rat. These results strongly suggest an important role for mitochondrial Mn-SOD as a potential end effector of this protection.

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Section: Cardioprotective Role Of Mn-sodmentioning

confidence: 99%

Adenosine A ₁ Receptor Activation Induces Delayed Preconditioning in Rats Mediated by Manganese Superoxide Dismutase

et al. 2000

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“…TNF-a or interleukin-1) [27,28]. This release of cytokines can further induce both the formation of oxygen radicals in granulocytes and the upregulation of FRSE activities in granulocytes [29]. We hypothesized that if haemodialysis therapy is associated with an increased production of oxygen radicals or cytokines, FRSE activity should be acutely regulated in granulocytes, thus protecting the cells against oxygen-radical-mediated injury.…”

Section: Statisticsmentioning

confidence: 99%

Oxidative stress during dialysis: effect on free radical scavenging enzyme (FRSE) activities and glutathione (GSH) concentration in granulocytes

Schettler

Wieland²,

Methe³

et al. 1998

Nephrology Dialysis Transplantation

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Abstractpromised as shown by decreased GSH concentrations, both suggesting increased oxidative stress. Background. Living cells are protected by free radical scavenging enzymes against oxygen radical-mediated damage. It has been suggested that granulocytes are Key words: extracorporeal circulation; free radical activated on the surface of dialyser membranes, scavenging enzyme activity; granulocyte; haemofiltraresulting in the generation of free radicals. We have tion; haemodialysis; oxygen radicals recently reported a lack of plasma lipid peroxidation and unchanged glutathione peroxidase (GSH-Px) as well as glutathione reductase (GSSG-R) activities in Introduction red blood cells of haemodialysis patients. However, because mature red cells are free of DNA and RNA, Oxygen radicals are toxic and are thought to be free radical scavenging enzymes (FRSE ) cannot be involved in the pathogenesis of a variety of diseases regulated on the gene level in response to an acute including chronic renal failure (CRF ) [1]. Haemooxidative stress. In contrast to erythrocytes, granulodialysis treatment has been suggested to impose an cytes are nucleated cells and FRSE protein concentraadditional oxidative stress to patients with CRF by tions can therefore be modulated.activation of granulocytes on dialyser membranes [1-3] Methods. GSH-Px, GSSG-R, superoxide dismutase or the energy of light to which blood components are (SOD) activities and total glutathione (GSH ) were usually not exposed under physiological conditions [4]. determined spectrophotometrically using a Cobas Fara Granulocytes take part in inflammatory reactions in semi-automatic analyser in granulocytes of 31 healthy the body. They are activated by mediators such as blood donors and in 28 patients with chronic renal cytokines or arachidonic acid metabolites to perform failure (CRF ) for more than 6 months before as well their phagocytic inflammatory reactions. Once activas immediately after a single dialysis treatment.ated, they undergo a respiratory burst with the conPatients were treated either by haemodialysis (n=17) comitant release of oxygen-derived free radicals using low-flux polysulphone membranes or by haeincluding superoxide anion (O 2 −), hydrogen peroxide mofiltration (n=11) usings high-flux polysulphone (H 2 O 2 ), hydroxyl radicals (OH ), and hypochlorous membranes.acid (HOCl ). Indiscriminate activation of granulocytes Results. Compared to healthy controls, SOD and leads to tissue damage shown as oxidation of lipid GSSG-R activities were increased in granulocytes of membranes of adjacent cells [5,6 ] as well as of granulo-HD and HF patients, GSH and GSH-Px were cytes themselves [7]. Former investigations indicated a decreased before a single treatment. After dialysis SOD dysfunction of granulocytes in patients undergoing and GSH-PX activities were significantly induced by long-term haemodialysis [8,9]. both HD and HF whereas GSSG-R activities andThe release of oxygen radicals from granulocytes GSH were decreased.has been suggested to be involved in the ...

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“…The generation of ROI and NO is regulated by multiple cytokines (9,13). Among them, granulocyte-macrophage colonystimulating factor (GM-CSF), interferons, and prostaglandins strongly induce NO synthase (NOS) (11,22,46) and activate other enzymes associated with ROI generation (27,39,41). However, the virulence of blastoconidia is correlated with their resistance to phagocytes (24).…”

mentioning

confidence: 99%

Lactoferrin Peptide Increases the Survival of Candida albicans - Inoculated Mice by Upregulating Neutrophil and Macrophage Functions, Especially in Combination with Amphotericin B and Granulocyte-Macrophage Colony-Stimulating Factor

et al. 2001

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To develop a new strategy to control candidiasis, we examined in vivo the anticandidal effects of a synthetic lactoferrin peptide, FKCRRWQWRM (peptide 2) and the peptide that mimics it, FKARRWQWRM (peptide 2). Although all mice that underwent intraperitoneal injection of 5 ؋ 10 8 Candida cells with or without peptide 2 died within 8 or 7 days, respectively, the survival times of mice treated with 5 to 100 g of intravenous peptide 2 per day for 5 days after the candidal inoculation were prolonged between 8.4 ؎ 2.9 and 22.4 ؎ 3.6 days, depending on the dose of peptide 2. The prolongation of survival by peptide 2 was also observed in mice that were infected with 1.0 ؋ 10 9 Candida albicans cells (3.2 ؎ 1.3 days in control mice versus 8.2 ؎ 2.4 days in the mice injected with 10 g of peptide 2 per day). In the high-dose inoculation, a combination of peptide 2 (10 g/day) with amphotericin B (0.1 g/day) and granulocyte-macrophage colony-stimulating factor (GM-CSF) (0.1 g/day) brought prolonged survival. With a combination of these agents, 60% of the mice were alive for more than 22 days. Correspondingly, peptide 2 activated phagocytes inducing inducible NO synthase and the expression of p47 phox and p67 phox , and peptide 2 increased phagocyte Candida-killing activities up to 1.5-fold of the control levels upregulating the generation of superoxide, lactoferrin, and defensin from neutrophils and macrophages. These findings indicated that the anticandidal effects of peptide 2 depend not only on the direct Candida cell growth-inhibitory activity, but also on the phagocytes' upregulatory activity, and that combinations of peptide 2 with GM-CSF and antifungal drugs will help in the development of new strategies for control of candidiasis.

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Role of Cytokines, Tyrosine Kinase, and Protein Kinase C on Production of Superoxide and Induction of Scavenging Enzymes in Human Leukocytes

Cited by 58 publications

References 0 publications

Adenosine A ₁ Receptor Activation Induces Delayed Preconditioning in Rats Mediated by Manganese Superoxide Dismutase

Adenosine A ₁ Receptor Activation Induces Delayed Preconditioning in Rats Mediated by Manganese Superoxide Dismutase

Oxidative stress during dialysis: effect on free radical scavenging enzyme (FRSE) activities and glutathione (GSH) concentration in granulocytes

Lactoferrin Peptide Increases the Survival of Candida albicans - Inoculated Mice by Upregulating Neutrophil and Macrophage Functions, Especially in Combination with Amphotericin B and Granulocyte-Macrophage Colony-Stimulating Factor

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Role of Cytokines, Tyrosine Kinase, and Protein Kinase C on Production of Superoxide and Induction of Scavenging Enzymes in Human Leukocytes

Cited by 58 publications

References 0 publications

Adenosine A 1 Receptor Activation Induces Delayed Preconditioning in Rats Mediated by Manganese Superoxide Dismutase

Adenosine A 1 Receptor Activation Induces Delayed Preconditioning in Rats Mediated by Manganese Superoxide Dismutase

Oxidative stress during dialysis: effect on free radical scavenging enzyme (FRSE) activities and glutathione (GSH) concentration in granulocytes

Lactoferrin Peptide Increases the Survival of Candida albicans - Inoculated Mice by Upregulating Neutrophil and Macrophage Functions, Especially in Combination with Amphotericin B and Granulocyte-Macrophage Colony-Stimulating Factor

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Adenosine A ₁ Receptor Activation Induces Delayed Preconditioning in Rats Mediated by Manganese Superoxide Dismutase

Adenosine A ₁ Receptor Activation Induces Delayed Preconditioning in Rats Mediated by Manganese Superoxide Dismutase