Skip to main content
Hauptrubriken
CME Facharzt-Training Webinare Zeitschriften Bücher e.Medpedia Podcast
Service
Jobbörse Info & Hilfe
Fachgebiete
Anästhesiologie Allgemeinmedizin Arbeitsmedizin Augenheilkunde Chirurgie Dermatologie Gynäkologie und Geburtshilfe HNO Innere Medizin Kardiologie Neurologie Onkologie und Hämatologie Orthopädie und Unfallchirurgie Pädiatrie Pathologie Psychiatrie Radiologie Rechtsmedizin Urologie Zahnmedizin
Themen
Klimawandel und Gesundheit Neues aus dem Markt COVID-19 Praxis und Beruf Seltene Erkrankungen GOÄ & EBM Panorama
Sammlungen
Kasuistiken Algorithmen & Infografiken Blickdiagnosen Arthropedia FlapFinder (für Dermatochirurgen) Videos Kongressberichterstattung Medizin für Apothekerinnen und Apotheker Für Ärztinnen und Ärzte in Weiterbildung Für Medizinstudierende
Erweiterte Suche
Anmelden
nach oben
Inflammation
Erschienen in: Inflammation 2/2014

01.04.2014

An Alternative Pathway Through the Fenton Reaction for the Formation of Advanced Oxidation Protein Products, a New Class of Inflammatory Mediators

verfasst von: Guilherme Vargas Bochi, Vanessa Dorneles Torbitz, Lara Peruzzolo Cargnin, José Antonio Mainardi de Carvalho, Patrícia Gomes, Rafael Noal Moresco

Erschienen in: Inflammation | Ausgabe 2/2014

Einloggen, um Zugang zu erhalten

Abstract

The accumulation of advanced oxidation protein products (AOPPs) has been linked to several pathological conditions, and their levels are formed during oxidative stress as a result of reactions between plasma proteins and chlorinated oxidants produced by myeloperoxidase (MPO). However, it was suggested that the generation of this mediator of inflammation may also occur via an MPO-independent pathway. The aim of this study was to induce the formation of AOPPs in vitro through Fenton reaction and to investigate whether this generation could be counteracted by N-acetylcysteine (NAC) and fructose-1,6-bisphosphate (FBP). The complete Fenton system increased the AOPPs levels and both NAC and FBP were capable of inhibiting the formation of Fenton reaction-induced AOPPs. These data provide a new hypothesis about another pathway of AOPPs formation, as well as report that NAC and FBP may be good candidates to neutralize pro-inflammatory and pro-oxidant effects of AOPPs in several diseases.
Literatur
1.
Halliwell, B. 2012. Free radicals and antioxidants: updating a personal view. Nutrition Reviews 70: 257–265.PubMedCrossRef
2.
Ray, P.D., B.W. Huang, and Y. Tsuji. 2012. Reactive oxygen species (ROS) homeostasis and redox regulation in cellular signaling. Cellular Signalling 24: 981–990.PubMedCentralPubMedCrossRef
3.
Sorescu, D., D. Weiss, B. Lassegue, R.E. Clempus, K. Szocs, G.P. Sorescu, L. Valppu, M.T. Quinn, J.D. Lambeth, J.D. Vega, W.R. Taylor, and K.K. Griendling. 2002. Superoxide production and expression of nox family proteins in human atherosclerosis. Circulation 105: 1429–1435.PubMedCrossRef
4.
Brownlee, M. 2001. Biochemistry and molecular cell biology of diabetic complications. Nature 414: 813–820.PubMedCrossRef
5.
Kaneda, H., J. Taguchi, K. Ogasawara, T. Aizawa, and M. Ohno. 2002. Increased level of advanced oxidation protein products in patients with coronary artery disease. Atherosclerosis 162: 221–225.PubMedCrossRef
6.
Kalousova, M., J. Skrha, and T. Zima. 2002. Advanced glycation end-products and advanced oxidation protein products in patients with diabetes mellitus. Physiological Research 51: 597–604.PubMed
7.
Witko-Sarsat, V., M. Friedlander, C. Capeillere-Blandin, T. Nguyen-Khoa, A.T. Nguyen, J. Zingraff, P. Jungers, and B. Descamps-Latscha. 1996. Advanced oxidation protein products as a novel marker of oxidative stress in uremia. Kidney International 49: 1304–1313.PubMedCrossRef
8.
Guo, Z.J., H.X. Niu, F.F. Hou, L. Zhang, N. Fu, R. Nagai, X. Lu, B.H. Chen, Y.X. Shan, J.W. Tian, R.H. Nagaraj, D. Xie, and X. Zhang. 2008. Advanced oxidation protein products activate vascular endothelial cells via a RAGE-mediated signaling pathway. Antioxidants and Redox Signaling 10: 1699–1712.PubMedCrossRef
9.
Zhou, L.L., W. Cao, C. Xie, J. Tian, Z. Zhou, Q. Zhou, P. Zhu, A. Li, Y. Liu, T. Miyata, F.F. Hou, and J. Nie. 2012. The receptor of advanced glycation end products plays a central role in advanced oxidation protein products-induced podocyte apoptosis. Kidney International 82: 759–770.PubMedCrossRef
10.
Himmelfarb, J., and E. McMonagle. 2001. Albumin is the major plasma protein target of oxidant stress in uremia. Kidney International 60: 358–363.PubMedCrossRef
11.
Mera, K., M. Anraku, K. Kitamura, K. Nakajou, T. Maruyama, and M. Otagiri. 2005. The structure and function of oxidized albumin in hemodialysis patients: Its role in elevated oxidative stress via neutrophil burst. Biochemical and Biophysical Research Communications 334: 1322–1328.PubMedCrossRef
12.
Shi, X.Y., F.F. Hou, H.X. Niu, G. Wang, D. Xie, Z.J. Guo, Z.M. Zhou, F. Yang, J.W. Tian, and X. Zhang. 2008. Advanced oxidation protein products promote inflammation in diabetic kidney through activation of renal nicotinamide adenine dinucleotide phosphate oxidase. Endocrinology 149: 1829–1839.PubMedCrossRef
13.
Zhou, L.L., F.F. Hou, G.B. Wang, F. Yang, D. Xie, Y.P. Wang, and J.W. Tian. 2009. Accumulation of advanced oxidation protein products induces podocyte apoptosis and deletion through NADPH-dependent mechanisms. Kidney International 76: 1148–1160.PubMedCrossRef
14.
Hanasand, M., R. Omdal, K.B. Norheim, L.G. Gøransson, C. Brede, and G. Jonsson. 2012. Improved detection of advanced oxidation protein products in plasma. Clinica Chimica Acta 413: 901–906.CrossRef
15.
Capeillère-Blandin, C., V. Gausson, B. Descamps-Latscha, and V. Witko-Sarsat. 2004. Biochemical and spectrophotometric significance of advanced oxidized protein products. Biochimica et Biophysica Acta 1689: 91–102.PubMedCrossRef
16.
Capeillère-Blandin, C., V. Gausson, A.T. Nguyen, B. Descamps-Latscha, T. Drüeke, and V. Witko-Sarsat. 2006. Respective role of uraemic toxins and myeloperoxidase in the uraemic state. Nephrology, dialysis, transplantation: official publication of the European Dialysis and Transplant Association – European Renal Association 21: 1555–1563.CrossRef
17.
Bochi, G.V., V.D. Torbitz, L.P. Cargnin, M.B. Sangoi, R.C. Santos, P. Gomes, and R.N. Moresco. 2012. Fructose-1,6-bisphosphate and N-acetylcysteine attenuate the formation of advanced oxidation protein products, a new class of inflammatory mediators, in vitro. Inflammation 35: 1786–1792.PubMedCrossRef
18.
Holmes, R.S., and C.J. Masters. 1970. Epigenetic interconversion of the multiple forms of mouse liver catalase. FEBS Letters 11: 45–48.PubMedCrossRef
19.
Witko-Sarsat, V., T. Nguyen Khoa, P. Jungers, T. Drüeke, and B. Descamps-Latscha. 1998. Advanced oxidation protein products: oxidative stress markers and mediators of inflammation in uremia. Advances in nephrology from the Necker Hospital 28: 321–341.PubMed
20.
Kalousová, M., J. Skrha, and T. Zima. 2002. Advanced glycation end-products and advanced oxidation protein products in patients with diabetes mellitus. Physiological Research 51: 597–604.PubMed
21.
Martín-Gallán, P., A. Carrascosa, M. Gussinyé, and C. Domínguez. 2003. Biomarkers of diabetes-associated oxidative stress and antioxidant status in young diabetic patients with or without subclinical complications. Free Radical Biology and Medicine 34: 1563–1574.PubMedCrossRef
22.
Tabak, O., R. Gelisgen, H. Erman, F. Erdenen, C. Muderrisoglu, H. Aral, and H. Uzun. 2011. Oxidative lipid, protein, and DNA damage as oxidative stress markers in vascular complications of diabetes mellitus. Clinical and Investigative Medicine 34: 163–171.
23.
Chen, S., L. Liu, X. Sun, Y. Liu, and T. Son. 2005. Captopril restores endothelium-dependent relaxation induced by advanced oxidation protein products in rat aorta. Journal of Cardiovascular Pharmacology 46: 803–809.PubMedCrossRef
24.
Drüeke, T., V. Witko-Sarsat, Z. Massy, B. Descamps-Latscha, A.P. Guerin, S.J. Marchais, V. Gausson, and G.M. London. 2002. Iron therapy, advanced oxidation protein products, and carotid artery intima-media thickness in end-stage renal disease. Circulation 106: 2212–2217.PubMedCrossRef
25.
Anraku, M., K. Kitamura, R. Shintomo, K. Takeuchi, H. Ikeda, J. Nagano, T. Ko, K. Mera, K. Tomita, and M. Otagiri. 2008. Effect of intravenous iron administration frequency on AOPP and inflammatory biomarkers in chronic hemodialysis patients: a pilot study. Clinical Biochemistry 41: 1168–1174.PubMedCrossRef
26.
Halliwell, B. 1978. Superoxide-dependent formation of hydroxyl radicals in the presence of iron salts. Its role in degradation of hyaluronic acid by a superoxide-generating system. FEBS Letters 96: 238–242.PubMedCrossRef
27.
Rooyakkers, T.M., E.S. Stroes, M.P. Kooistra, E.E. Van Faassen, R.C. Hider, T.J. Rabelink, and J.J. Marx. 2002. Ferric saccharate induces oxygen radical stress and endothelial dysfunction in vivo. European Journal of Clinical Investigation 32: 9–16.PubMedCrossRef
28.
Tovbin, D., D. Mazor, M. Vorobiov, C. Chaimovitz, and N. Meyerstein. 2002. Induction of protein oxidation by intravenous iron in hemodialysis patients: Role of inflammation. American Journal of Kidney Diseases 40: 1005–1012.PubMedCrossRef
29.
Stępniak, J., A. Lewiński, and M. Karbownik-Lewińska. 2013. Membrane lipids and nuclear DNA are differently susceptive to Fenton reaction substrates in porcine thyroid. Toxicology In Vitro 27: 71–78.PubMedCrossRef
30.
Valko, M., C.J. Rhodes, J. Moncol, M. Izakovic, and M. Mazur. 2006. Free radicals, metals and antioxidants in oxidative stress-induced cancer. Chemico-Biological Interactions 160: 1–40.PubMedCrossRef
31.
Repka, T., and R.P. Hebbel. 1991. Hydroxyl radical formation by sickle erythrocyte membranes: Role of pathologic iron deposits and cytoplasmic reducing agents. Blood 78: 2753–2758.PubMed
32.
Trachootham, D., W. Lu, M.A. Ogasawara, R.D. Nilsa, and P. Huang. 2008. Redox regulation of cell survival. Antioxidants and Redox Signaling 10: 1343–1374.PubMedCentralPubMedCrossRef
33.
Pellegrino, P., B. Mallet, S. Delliaux, Y. Jammes, R. Gieu, and O. Schaf. 2011. Zeolites are effective ROS-scavengers in vitro. Biochemical and Biophysical Research Communications 410: 478–483.PubMedCrossRef
34.
Witko-Sarsat, V., V. Gausson, A.T. Nguyen, M. Touam, T. Drüeke, F. Santangelo, and B. Descamps-Latscha. 2003. AOPP-induced activation of human neutrophil and monocyte oxidative metabolism: A potential target for N-acetylcysteine treatment in dialysis patients. Kidney International 64: 82–91.PubMedCrossRef
35.
Aruoma, O.I., B. Halliwell, B.M. Hoey, and J. Butler. 1989. The antioxidant action of N-acetylcysteine: Its reaction with hydrogen peroxide, hydroxyl radical, superoxide, and hypochlorous acid. Free Radical Biology and Medicine 6: 593–597.PubMedCrossRef
36.
Fishbane, S. 2008. N-Acetylcysteine in the prevention of contrast-induced nephropathy. Clinical Journal of the American Society of Nephrology 3: 281–287.PubMedCrossRef
37.
Holt, S., R. Marley, B. Fernando, D. Harry, R. Anand, D. Goodier, and K. Moore. 1999. Acute cholestasis-induced renal failure: Effects of antioxidants and ligands for the thromboxane A2 receptor. Kidney International 55: 271–277.PubMedCrossRef
38.
Santos, R.C., R.N. Moresco, M.A. Peña Rico, A.R. Susperregui, J.L. Rosa, R. Bartrons, F. Ventura, D.N. Mário, S.H. Alves, E. Tatsch, H. Kober, R.O. de Mello, P. Scherer, H.B. Dias, and J.R. de Oliveira. 2012. Fructose-1,6-bisphosphate reduces the mortality in Candida albicans bloodstream infection and prevents the septic-induced platelet decrease. Inflammation 35: 1256–1261.PubMedCrossRef
39.
de Mello, R.O., A. Lunardelli, E. Caberlon, C.M. de Moraes, R. Christ Vianna Santos, V.L. da Costa, G.V. da Silva, P. da Silva Scherer, L.E. Buaes, D.A. da Silva Melo, M.V. Donadio, F.B. Nunes, and J.R. de Oliveira. 2011. Effect of N-acetylcysteine and fructose-1,6-bisphosphate in the treatment of experimental sepsis. Inflammation 34: 539–550.PubMedCrossRef
40.
Alva, N., T. Carbonell, T. Roig, J. Bermúdez, and J. Palomeque. 2011. Fructose 1,6 biphosphate administration to rats prevents metabolic acidosis and oxidative stress induced by deep hypothermia and rewarming. European Journal of Pharmacology 659: 259–264.PubMedCrossRef
41.
Bajić, A., J. Zakrzewska, D. Godjevac, P. Andjus, D.R. Jones, M. Spasić, and I. Spasojević. 2011. Relevance of the ability of fructose 1,6-bis(phosphate) to sequester ferrous but not ferric ions. Carbohydrate Research 346: 416–420.PubMedCrossRef
42.
Wei, X.F., Q.G. Zhou, F.F. Hou, B.Y. Liu, and M. Liang. 2009. Advanced oxidation protein products induce mesangial cell perturbation through PKC-dependent activation of NADPH oxidase. American Journal of Physiology. Renal Physiology 296: 427–437.CrossRef
43.
Zhou, Q.G., M. Zhou, A.J. Lou, D. Xie, and F.F. Hou. 2010. Advanced oxidation protein products induce inflammatory response and insulin resistance in cultured adipocytes via induction of endoplasmic reticulum stress. Cellular physiology and biochemistry: international journal of experimental cellular physiology, biochemistry, and pharmacology 26: 775–786.CrossRef
44.
Cao, W., J. Xu, Z.M. Zhou, G.B. Wang, F.F. Hou, and J. Nie. 2013. Advanced oxidation protein products activate intrarenal renin–angiotensin system via a CD36-mediated, redox-dependent pathway. Antioxidants and Redox Signaling 18: 19–35.PubMedCentralPubMedCrossRef
45.
Valente, A.J., T. Yoshida, R.A. Clark, P. Delafontaine, U. Siebenlist, and B. Chandrasekar. 2013. Advanced oxidation protein products induce cardiomyocyte death via Nox2/Rac1/superoxide-dependent TRAF3IP2/JNK signaling. Free Radical Biology and Medicine 60: 125–135.PubMedCrossRef
46.
Prousek, J. 2007. Fenton chemistry in biology and medicine. Pure and applied chemistry 79: 2325–2338.CrossRef
47.
Repetto, M.G., N.F. Ferrarotti, and A. Boveris. 2010. The involvement of transition metal ions on iron-dependent lipid peroxidation. Archives of Toxicology 84: 255–262.PubMedCrossRef
48.
González, F.B., S. Llesuy, and A. Boveris. 1991. Hydroperoxide-initiated chemiluminescence: Assay for oxidative stress in biopsies of heart, liver and muscle. Free Radical Biology and Medicine 10: 93–100.CrossRef
49.
Chance, B., H. Sies, and A. Boveris. 1979. Hydroperoxide metabolism in mammalian organs. Physiological Reviews 59: 527–605.PubMed
50.
Marsche, G., S. Frank, A. Hrzenjak, M. Holzer, S. Dirnberger, C. Wadsack, H. Scharnagl, T. Stojakovic, A. Heinemann, and K. Oettl. 2009. Plasma-advanced oxidation products are potent high-density lipoprotein receptor antagonists in vivo. Circulation Research 104: 750–757.
Metadaten
Titel
An Alternative Pathway Through the Fenton Reaction for the Formation of Advanced Oxidation Protein Products, a New Class of Inflammatory Mediators
verfasst von
Guilherme Vargas Bochi
Vanessa Dorneles Torbitz
Lara Peruzzolo Cargnin
José Antonio Mainardi de Carvalho
Patrícia Gomes
Rafael Noal Moresco
Publikationsdatum
01.04.2014
Verlag
Springer US
Erschienen in
Inflammation / Ausgabe 2/2014
Print ISSN: 0360-3997
Elektronische ISSN: 1573-2576
DOI
https://doi.org/10.1007/s10753-013-9765-1

Weitere Artikel der Ausgabe 2/2014

Inflammation 2/2014 Zur Ausgabe

OriginalPaper

Pharmacokinetic and Anti-inflammatory Effects of Sanguinarine Solid Lipid Nanoparticles

OriginalPaper

IL-6 Trans-Signaling Enhances CCL20 Production from IL-1β-Stimulated Human Periodontal Ligament Cells

OriginalPaper

Netrin-1 Attenuates Cardiac Ischemia Reperfusion Injury and Generates Alternatively Activated Macrophages

OriginalPaper

Selenium Inhibits LPS-Induced Pro-inflammatory Gene Expression by Modulating MAPK and NF-κB Signaling Pathways in Mouse Mammary Epithelial Cells in Primary Culture

OriginalPaper

Long-Term Stability of Uveitis with Faint Anterior Chamber Flare Treated with Once-Daily Topical Ophthalmic Betamethasone

OriginalPaper

Cepharanthine Attenuates Lipopolysaccharide-Induced Mice Mastitis by Suppressing the NF-κB Signaling Pathway

Leitlinien kompakt für die Innere Medizin

Mit medbee Pocketcards sicher entscheiden.

Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag

Kostenlos registrieren

Neu im Fachgebiet Innere Medizin

Notfall-TEP der Hüfte ist auch bei 90-Jährigen machbar

26.04.2024 Hüft-TEP Nachrichten

Ob bei einer Notfalloperation nach Schenkelhalsfraktur eine Hemiarthroplastik oder eine totale Endoprothese (TEP) eingebaut wird, sollte nicht allein vom Alter der Patientinnen und Patienten abhängen. Auch über 90-Jährige können von der TEP profitieren.

Niedriger diastolischer Blutdruck erhöht Risiko für schwere kardiovaskuläre Komplikationen

25.04.2024 Hypotonie Nachrichten

Wenn unter einer medikamentösen Hochdrucktherapie der diastolische Blutdruck in den Keller geht, steigt das Risiko für schwere kardiovaskuläre Ereignisse: Darauf deutet eine Sekundäranalyse der SPRINT-Studie hin.

Bei schweren Reaktionen auf Insektenstiche empfiehlt sich eine spezifische Immuntherapie

25.04.2024 Allergien und Intoleranzreaktionen Nachrichten

Insektenstiche sind bei Erwachsenen die häufigsten Auslöser einer Anaphylaxie. Einen wirksamen Schutz vor schweren anaphylaktischen Reaktionen bietet die allergenspezifische Immuntherapie. Jedoch kommt sie noch viel zu selten zum Einsatz.

Therapiestart mit Blutdrucksenkern erhöht Frakturrisiko

25.04.2024 Hypertonie Nachrichten

Beginnen ältere Männer im Pflegeheim eine Antihypertensiva-Therapie, dann ist die Frakturrate in den folgenden 30 Tagen mehr als verdoppelt. Besonders häufig stürzen Demenzkranke und Männer, die erstmals Blutdrucksenker nehmen. Dafür spricht eine Analyse unter US-Veteranen.

Update Innere Medizin

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.

Newsletter bestellen
Bildnachweise