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1

The mystery of reactive oxygen species derived from cell respiration

100%

Nohl H., Gille L., Staniek K.

Acta Biochimica Polonica

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2004

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tom 51

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nr 1

Mitochondrial respiration is considered to provide reactive oxygen species (ROS) as byproduct of regular electron transfer. Objections were raised since results obtained with isolated mitochondria are commonly transferred to activities of mitochondria in the living cell. High electrogenic membrane potential was reported to trigger formation of mitochondrial ROS involving complex I and III. Suggested bioenergetic parameters, starting ROS formation, widely change with the isolation mode. ROS detection systems generally applied may be misleading due to possible interactions with membrane constituents or electron carriers. Avoiding these problems no conditions reported to transform mitochondrial respiration to a radical source were confirmed. However, changing the physical membrane state affected the highly susceptible interaction of the ubiquinol/&C1 redox complex such that ROS formation became possible.

2

Scavenging of oxygen radicals by heme peroxidases

100%

Gebicka L., Gebicki J. L.

Acta Biochimica Polonica

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1996

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tom 43

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nr 4

The reactions of two heme peroxidases, horseradish peroxidase and lactoperoxidase and their compounds II (oxoferryl heme intermediates, Fe(IV)=0 or ferric protein radical Fe(III)R') and compounds III (resonance hybrids [Fe(IIIK)2 «-» Fe(II)-02l with superoxide radical anion generated enzymatically or radiolytically, and with hydroxyl radicals generated radiolytically, were investigated. It is suggested that only the protein radical form of compound II of lactoperoxidase reacts with superoxide, whereas compound II of horseradich peroxidase, which exists only in oxoferryl form, is unreactive towards superoxide. Compound III of the investigated peroxidases does not react with superoxide. The lactoperoxidase activity loss induced by hydroxyl radicals is closely related to the loss of the ability to form compound I (oxoferryl porphyrin n-cation radical, Fed V)=0(Por+) or oxoferryl protein radical Fe(IV)=0(R )). On the other hand, the modification of horseradish peroxidase induced by hydroxyl radicals has been reported to cause also restrictions in substrate binding (Gębicka, L. & Gębicki, J.L., 1996, Biochimie 78,62-65). Nevertheless, it has been found that only a small fraction of hydroxyl radicals generated homogeneously does inactivate the enzymes.

3

Nitric oxide and superoxide in inflammation and immune regulation

100%

Guzik T. J., Korbut R., Adamek-Guzik T.

Journal of Physiology and Pharmacology

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2003

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tom 54

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nr 4

Nitric oxide (NO) and reactive oxygen species exert multiple modulating effects on inflammation and play a key role in the regulation of immune responses. They affect virtually every step of the development of inflammation. Low concentrations of nitric oxide produced by constitutive and neuronal nitric oxide synthases inhibit adhesion molecule expression, cytokine and chemokine synthesis and leukocyte adhesion and transmigration. Large amounts of NO, generated primarily by iNOS can be toxic and pro-inflammatory. Actions of nitric oxide are however not dependent primarily on the enzymatic source, but rather on the cellular context, NO concentration (dependent on the distance from NO source) and initial priming of immune cells. These observations may explain difficulties in determining the exact role of NO in Th1 and Th2 lymphocyte balance in normal immune responses and in allergic disease. Similarly superoxide anion produced by NAD(P)H oxidases present in all cell types participating in inflammation (leukocytes, endothelial and other vascular cells etc) may lead to toxic effects, when produced at high levels during oxidative burst, but may also modulate inflammation in a far more discrete way, when continuously produced at low levels by NOXs (non-phagocytic oxidases). The effects of both nitric oxide and superoxide in immune regulation are exerted through multiple mechanisms, which include interaction with cell signalling systems like cGMP, cAMP, G-protein, JAK/STAT or MAPK dependent signal transduction pathways. They may also lead to modification of transcription factors activity and in this way modulate the expression of multiple other mediators of inflammation. Moreover genetic polymorphisms exist within genes encoding enzymes producing both NO and superoxide. The potential role of these polymorphisms in inflammation and susceptibility to infection is discussed. Along with studies showing increasing role of NO and free radicals in mediating inflammatory responses drugs which interfere with these systems are being introduced in the treatment of inflammation. These include statins, angiotensin receptor blockers, NAD(P)H oxidase inhibitors, NO-aspirin and others. In conclusion in this mini-review we discuss the mechanisms of nitric oxide and superoxide dependent modulation of inflammatory reactions in experimental animals and humans. We also discuss potential roles of nitric oxide as a mediator of allergic inflammation.

4

Peroxynitrite mediator of the toxic action of nitric oxide

84%

Bartosz G.

Acta Biochimica Polonica

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1996

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tom 43

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nr 4

Peroxynitrite (oxoperoxonitrate(-l)), anion of peroxynitrous acid, is thought to mediate the toxic action of nitric oxide and superoxide anion. Peroxynitrite is formed in a fast reaction between these species, reacts with all classes of biomolecules, is cytotoxic, and is thought to be involved in many pathological phenomena. Its main reactions involve one- and two-electron oxidation and nitration. Protein nitration is often used as a footprint of peroxynitrite reactions in vivo. Nitration of tyrosine and of tyrosyl residues in proteins may be an important mechanism of derangement of biochemical signal transduction by this compound. However, apparently beneficial effects of peroxynitrite have also been described, among them formation of nitric oxide and nitric oxide donors in reactions of peroxynitrite with thiols and alcohols.

5

Endothelial NADH-NADPH-dependent enzymatic sources of superoxide production: relationship to endothelial dysfunction

84%

Kalinowski L., Malinski T.

Acta Biochimica Polonica

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2004

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tom 51

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nr 2

There is growing evidence that endothelial dysfunction, which is often defined as the decreased endothelial-derived nitric oxide (NO) bioavailability, is a crucial factor leading to vascular disease states such as hypertension, diabetes, atherosclerosis, heart failure and cigarette smoking. This is due to the fact that the lack of NO in en- dothelium-dependent vascular disorders contributes to impaired vascular relaxation, platelet aggregation, increased vascular smooth muscle proliferation, and enhanced leukocyte adhesion to the endothelium. During the last several years, it has become clear that reduction of NO bioavailability in the endothelium-impaired function disorders is associated with an increase in endothelial production of superoxide (O2 ). Because O2 - rapidly scavenges NO within the endothelium, a reduction of bioactive NO might occur despite an increased NO generation. Among many enzymatic systems that are capable of producing O2 -, NAD(P)H oxidase and uncoupled endothelial NO synthase (eNOS) apparently are the main sources of O2- in the endothelialcells. It seems that O2– generated by NAD(P)H oxidase may trigger eNOS uncoupling and contribute to the endothelial balance between NO and O2–. That is maintained at diverse levels.

6

Superoxide- and nitric oxide-derived species mediate endothelial dysfunction, endothelial glycocalyx disruption, and enhanced neutrophil adhesion in the post-ischemic guinea-pig heart

84%

Kurzelewski M., Czarnowska E., Baresewicz A.

Journal of Physiology and Pharmacology

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2005

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tom 56

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nr 2

The study was aimed at testing the hypothesis that a toxic product of the reaction between superoxide (O2-) and nitric oxide (NO) mediates, not only endothelial dysfunction, but also endothelium-glycocalyx disruption, and increased neutrophil (PMN) accumulation in the heart subjected to ischemia/reperfusion (IR) injury. Accordingly, we studied if scavengers of either O2- or NO, or a compound that was reported to attenuate cardiac production of peroxynitrite, would prevent endothelial injury and subsequent PNM adhesion in IR heart. Langendorff-perfused guinea-pig hearts were subjected to 30 min ischemia/35 min reperfusion, and infusion of PMN between 15 and 25 min of the reperfusion. Coronary flow responses to acetylcholine (ACh) and sodium nitroprusside (SNP) were used as measures of endothelium-dependent and -independent vascular function, respectively. PMN adhesion and endothelium glycocalyx ultrastructure were assessed in histological preparations. IR impaired the ACh, but not SNP, response by approximately 60%, caused endothelium-glycocalyx disruption, and approximately nine-fold increase in PMN adhesion. These alterations were prevented by superoxide dismutase (150 U/ml), NO synthase inhibitor, L-NAME (10 µM), NO scavenger, oxyhemoglobin (25 µM), and NO donor, SNAP (1 µM), and were not affected by catalase (600 u/ml). The glycocalyx-protective effect of these interventions preceded their effect on PMN adhesion. The data imply that PMN adhesion in IR guinea-pig heart is a process secondary to functional and/or structural changes in coronary endothelium, and that a toxic product of the reaction between superoxide and NO mediates these endothelial changes.

7

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The protective role of nitric oxide in the brain ischemia

84%

Dobrucki L. W., Kalinowski L., Uracz W., Malinski T.

Journal of Physiology and Pharmacology

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2000

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tom 51

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nr 4,1

8

Effect of cyclosporin A on immunological response in lungs of guinea pigs infected with Trichinella spiralis

84%

Dzik J. M., Zielinski Z., Golos B., Jagielska E., Wranicz M., Walajtys-Rode E.

Acta Biochimica Polonica

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2002

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tom 49

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nr 1

The effects of cyclosporin A (CsA), a potent immunosuppressive drug with antiparasitic activity, on the innate immunological response in guinea pig lungs during an early period (6th and 14th days) after T. spiralis infection were studied. CsA treatment of T. spiralis-infected guinea pigs caused a significant attenuation of immuno- logical response in lungs by decreasing lymphocyte infiltration into pulmonary alveolar space, inhibiting alveolar macrophage superoxide anion production and lowering both the production of NO metabolites measured in bronchoalveolar lavage fluid and expression of the iNOS protein in lung homogenates, allowing us to speculate that the T. spiralis-dependent immunological response is dependent on lymphocyte T function. Interestingly, CsA itself had a pro-inflammatory effect, promoting leucocyte accumulation and macrophage superoxide production in guinea pig lungs. This observation may have a relevance to the situation in patients undergoing CsA therapy. Macrophage expression of the iNOS protein, evaluated by immunoblotting was not influenced by treatment of animals with CsA or anti-TGF-antibody, indicating different regulation of the guinea pig and murine enzymes.

9

Perivascular adipose tissue as a messenger of the brain-vessel axis: role in vascular inflammation and dysfunction

84%

Guzik T. J., Marvar P. J., Czesnikiewicz-Guzik M., Korbut R.

Journal of Physiology and Pharmacology

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2007

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tom 58

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nr 4

10

Effect of leukotoxin of Mannheimia haemolytica and LPS of E. coli on secretory response of bovine neutrophils in vitro

67%

Wessely-Szponder J., Urban-Chmiel R., Wernicki A., Bobowiec R.

Polish Journal of Veterinary Sciences

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2005

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tom 08

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nr 2

11

Superoxide is a potential culprit of caspase-3 dependent endothelial cell death induced by lysophosphatidylcholine

67%

Park S., Kim J. A., Choi S., Suh S. A.

Journal of Physiology and Pharmacology

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2010

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tom 61

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nr 4

375-381

Oxidative stress in the vascular wall has intimately been implicated in the apoptosis of human umbilical vein endothelial cells (HUVECs) by lysophosphatidylcholine (LPC). However, the major type of reactive oxygen species (ROS) in this apoptotic signaling pathway remains to be clarified. In this study, we report that superoxide mediate LPC-induced caspase-3 dependent apoptosis in cultured HUVECs. The stimulation of HUVECs with LPC evoked apoptosis and ROS generation, and inhibited nitric oxide (NO) production in a dose-dependent manner. The classical caspase-3 dependent apoptosis was determined after 16 hours treatment by Western blotting using an antibody against cleaved caspase-3. The caspase-3 activation induced by LPC was prominently inhibited by antioxidants or NO donors and enhanced by NO inhibitors. Especially, LPC-induced caspase-3 activation was inhibited by superoxide dismutase (SOD) and enhanced by ammonium tetrathiomolybdate, SOD inhibitor. Additionally, xanthine/xanthine oxidase mixture increased the caspase-3 activation but catalase failed to reduce this superoxide-induced caspase-3 activation. These findings indicate that the superoxide generation caused by LPC activates the caspase-3 which results in HUVECs death. This study reveals some evidences linking superoxide with caspase-3 activation and provides a new dimension to superoxide-mediated caspase-3 activation in developing the endothelial dysfunction and atherosclerosis.

12

Generation of reactive oxygen species in plants during high light stress and their role in signaling

67%

Krieger-Liszkay A.

BioTechnologia. Journal of Biotechnology Computational Biology and Bionanotechnology

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2013

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tom 94

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nr 3

13

HD-Zip class III transcription factors control root development through the modulation of ROS levels

67%

Valdes A., Roberts C., Carlsbecker A.

BioTechnologia. Journal of Biotechnology Computational Biology and Bionanotechnology

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2013

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tom 94

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nr 2

14

A possible involvement of plasma membrane NAD[P]H oxidase in the switch mechanism of the cell death mode from apoptosis to necrosis in menadione-induced cell injury

67%

Niemczyk E., Majczak A., Hallmann A., Kedzior J., Wozniak M., Wakabayashi T.

Acta Biochimica Polonica

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2004

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tom 51

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nr 4

The effects of inhibitors of plasma membrane NADPH oxidase on menadione-induced cell injury processes were studied using human osteosarcoma 143B cells. The intracellular level of superoxide in the cells treated with menadione for 6 h reached a maximum followed by an abrupt decrease. The population of apoptotic cells detected by Annexin V and propidium iodide double staining also reached its maximum at 6 h of menadione-treatment while that of necrotic cells increased continuously reaching 90% of the total population at 9 h of the treatment. Pretreatment of the cells with inhibitors of NADPH oxidase, including diphenyliodonium chloride, apocynin, N-vani- llylnonanamide and staurosporine was effective in lowering the menadione-induced elevations of superoxide, and also in the suppression of the switch of the cell death mode from apoptosis to necrosis in menadione-treated cells except for the case of staurosporine. These results strongly suggest that superoxide generated by NADPH oxidase, besides that generated by the mitochondria, may contribute to the remarkable increase in the intracellular level of superoxide in the cells treated with menadione for 6 h resulting in the switch from apoptosis to necrosis, although a direct evidence of the presence of active and inactive forms of NADPH oxidase in control and menadione-treated 143B cells is lacking at present.

15

In situ measurement of nitric oxide, superoxide and peroxynitrite during endotoxemia

67%

Brovkovych V., Patton S., Brovkovych S., Kiechle F., Huk I., Malinski T.

Journal of Physiology and Pharmacology

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1997

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tom 48

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nr 4

16

Nitric oxide release from normal and dysfunctional endothelium

67%

Brovkovych V., Dobrucki L. W., Brovkovych S., Dobrucki I., Do Nascimento C. A., Burewicz A., Malinski T.

Journal of Physiology and Pharmacology

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1999

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tom 50

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nr 4

17

Elucidating structure-function relationships from molecule-to-cell-to-tissue: from research modalities to clinical realities

59%

Dobrucki L. W., Marsh B. J., Kalinowski L.

Journal of Physiology and Pharmacology. Supplement

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2009

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tom 60

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nr 4

Ograniczanie wyników

The mystery of reactive oxygen species derived from cell respiration

Scavenging of oxygen radicals by heme peroxidases

Nitric oxide and superoxide in inflammation and immune regulation

Peroxynitrite mediator of the toxic action of nitric oxide

Endothelial NADH-NADPH-dependent enzymatic sources of superoxide production: relationship to endothelial dysfunction

Superoxide- and nitric oxide-derived species mediate endothelial dysfunction, endothelial glycocalyx disruption, and enhanced neutrophil adhesion in the post-ischemic guinea-pig heart

The protective role of nitric oxide in the brain ischemia

Effect of cyclosporin A on immunological response in lungs of guinea pigs infected with Trichinella spiralis

Perivascular adipose tissue as a messenger of the brain-vessel axis: role in vascular inflammation and dysfunction

Effect of leukotoxin of Mannheimia haemolytica and LPS of E. coli on secretory response of bovine neutrophils in vitro

Superoxide is a potential culprit of caspase-3 dependent endothelial cell death induced by lysophosphatidylcholine

Generation of reactive oxygen species in plants during high light stress and their role in signaling

HD-Zip class III transcription factors control root development through the modulation of ROS levels

A possible involvement of plasma membrane NAD[P]H oxidase in the switch mechanism of the cell death mode from apoptosis to necrosis in menadione-induced cell injury

In situ measurement of nitric oxide, superoxide and peroxynitrite during endotoxemia

Nitric oxide release from normal and dysfunctional endothelium

Elucidating structure-function relationships from molecule-to-cell-to-tissue: from research modalities to clinical realities