Wissenschaftliches:


 http://www.uniklinik-duesseldorf.de/biochemie-und-molekularbiologieeins

Auf dem Forschungsgebiet oxidativer Stress ist das Institut für Biochemie und Molekularbiologie I Universitätsklinikum Düsseldorf international bekannt und in Kooperationen mit führenden Gruppen in den USA und Europa eingebunden. 

Forschungsschwerpunkt d. Instituts ist die Biochemie des oxidativen Stresses. Aerobe Stoffwechselvorgänge, photobiologische Effekte, körpereigene Abwehrprozesse und exogene Schadstoffe führen zur Bildung von reaktiven Sauerstoffverbindungen im Organismus. Darunter fallen auch die besonders reaktionsfreudigen freien Radikale, die biologisch wichtige Moleküle wie Lipide, DNA oder Proteine modifizieren oder zerstören können. 

Zur Aufklärung dieser Zusammenhänge werden Untersuchungen zu biochemischen Reaktionsmechanismen, genregulatorischen Effekten, zellulären Signalabläufen sowie biokinetische Untersuchungen und Interventionsstudien am Menschen durchgeführt. Ziel der Studien ist es, die Wirkmechanismen von reaktiven Sauerstoffverbindungen und freien Radikalen bei der Entstehung degenerativer Erkrankungen zu ermitteln und mit Hilfe von Antioxidantien Präventionsmöglichkeiten zu entwickeln.




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Ozonized Low Density Lipoprotein (ozLDL) Inhibits NF-kappaB and IRAK-1–Associated Signaling 
Original received November 12, 2005 
The aim of our study was to investigate whether LDL that is exposed to ozone before addition to cells, which we named ozLDL, is able to affect cellular functions. As a readout we used the NF-kappaB system as a paradigm for inflammatory signaling. Our data demonstrated that ozLDL and cholesterol ozonization products inhibited the activation of NF-kappaB in monocytic and endothelial cells stimulated by LPS, a prototypical inducer of innate immunity, as well as IL-1 receptor-associated kinase-1 (IRAK-1)–mediated signaling, whereas the TNF pathway was not affected.
(Arterioscler Thromb Vasc Biol. 2007;27:226-232.) Original received November 12, 2005; final version accepted September 28, 2006. From the Institute of Clinical Chemistry and Pathobiochemistry (C.C., B.S., A.Z., M.K., B.W., H.W.S., D.N., K.B.), Klinikum rechts der Isar, Technische Universität Muüchen, Germany; the Department of Restorative Dentistry and Periodontology (K.C.H.), Ludwig-Maximilians-Universitaä München, Germany; and INSERM U-545 and Institut Pasteur de Lille (C.F., M.R.), Lille, France. 
http://atvb.ahajournals.org/content/27/1/226.full.pdf

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Atherosclerosis. 2009 Aug:  
„We tested the hypothesis that administration of an 
oxygen/ozone mixture (IMT - immuno modulation therapy) might 
counteract the 
pathophysiological mechanism of Inflammatory mediators contributing to the impairment of vasculogenesis and enhancing limb tissue perfusion 
in patients with critical limb ischemia (CLI). 
RESULTS: TcPO(2) transcutaneous oxygen tension and CD34/CD133-positive cells increased at 22 weeks in IMT group (P<0.01) whereas no changes were observed in placebo group. TNF-alpha levels decreased at 6 months in IMT group (P<0.001) whereas no changes were observed in placebo group. There was a strong positive correlation between CD34/KDR-positive cells and TcPO(2) (r=0.56, P<0.01). Moreover, there was an inverse correlation between CD34/KDR-positive cells and TNF-alpha (r=-0.51, P<0.01). 
CONCLUSIONS: Intramuscular injection of IMT may improve wound healing and limb salvage in patients with CLI.
    BACKGROUND/AIMS: Inflammatory mediators contribute to the impairment of vasculogenesis by reducing endothelial progenitor cells (EPCs) mobilization in atherosclerotic vasculopathy. We tested the hypothesis that administration of an oxygen/ozone mixture (IMT) might counteract this pathophysiological mechanism and enhance limb tissue perfusion in patients with critical limb ischemia (CLI). METHODS: Randomized patients with rest pain or ischemic ulcers and transcutaneous oxygen tension (TcPO(2)) <40mmHg and/or toe pressure <50mmHg received placebo (n=74) or a non-specific immunomodulation therapy (IMT) (n=77), autologous blood exposed to oxygen/ozone gas mixture by intragluteal injection, on day 1, 2, 7, and once a week thereafter for at least 22 weeks. Patients were evaluated for changes in TcPO(2), levels of circulating EPCs (CD34/KDR-positive cells) and inflammation (tumor necrosis factor-alpha-TNF-alpha). RESULTS: TcPO(2) and CD34/CD133-positive cells increased at 22 weeks in IMT group (P<0.01) whereas no changes were observed in placebo group. TNF-alpha levels decreased at 6 months in IMT group (P<0.001) whereas no changes were observed in placebo group. There was a strong positive correlation between CD34/KDR-positive cells and TcPO(2) (r=0.56, P<0.01). Moreover, there was an inverse correlation between CD34/KDR-positive cells and TNF-alpha (r=-0.51, P<0.01). CONCLUSIONS: Intramuscular injection of IMT may improve wound healing and limb salvage in patients with CLI
Quelle: Atherosclerosis. 2009 Aug 8:Use of a non-specific immunomodulation therapy as a therapeutic vasculogenesis strategy in no-option critical limb ischemia patients. Marfella R, Luongo C, Coppola A, Luongo M, Capodanno P, Ruggiero R, Mascolo L, Ambrosino I, Sardu C, Boccardi V, Lettieri B, Paolisso G. Department of Geriatrics and Metabolic Diseases, Second University of Naples, Italy


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Dissertation an der Humbodt-Universität Berlin von 1998: 
Die Gewebeschädigung nach akuter Durchblutungsstörung im Gehirn 
(Ischämie/Reperfusion) Diese könnte durch sofortige Ozontherapie möglicherweise reduziert werden.

Mikroskopisch-morphologische und biochemische Nierenschäden nach künstlich gesetzter akuter Durchblutungsstörung bei Versuchstieren (Ratten) waren deutlich vermindert bei denjenigen Tieren, welche vorgängig 10 bis 15 Ozonbehandlungen erhalten hatten.
In der Dissertation an der Humbodt-Universität Berlin von 1998 wird auf die Prozesse bei Ischämie/Reperfusion im zentralen Nervensystem (ZNS) eingegangen. Dabei werden reaktive Sauerstoff-Spezies (ROS) als von zentraler Bedeutung eingestuft, weil sie die Blut-Hirn-Schranke während der Ischämie/Reperfusion bzw. Hypoxie/ Reoxygenierung zu öffnen vermögen und so für einen Teil der zerebralen Schädigung verantwortlich sind. 
(siehe: http://edoc.hu-berlin.de/dissertationen/medizin/schroeter-matthias/HTML/schroeter.html)

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2009 Jan 28; Department of Experimental Medicine, Faculty of Med. and Surgery, Second University of Naples
Chronisches Schmerzsyndrom (Allodynie):

The neuropathic pain model consisting of the spared nerve injury of the sciatic nerve was used in the mouse to examine whether peripheral neuropathy is capable of generating over-expression of pro-inflammatory and pro-apoptotic genes in the orbito-frontal cortex, together with allodynia and hyperalgesia. RT-PCR analysis showed increased expression of caspase-1, caspase-12 and caspase-8 genes in the orbito-frontal cortex 14 days after spared nerve injury of the sciatic nerve. Conversely, the expression of caspase-3 was decreased by spared nerve injury of the sciatic nerve in the same brain area. A single subcutaneous injection of ozone performed 12 h after the surgical procedure decreased mechanical allodynia and normalized the mRNA caspase-1, caspase-12 and caspase-8 gene levels, but did not the decrease caspase-3 level, 14 days post-spared nerve injury. Ozone also reduced IL-1beta staining in the orbito-frontal cortex in neuropathic mice. 
This study provides evidence that a single subcutaneous administration of ozone decreased neuropathic pain type behaviour, normalized the expression of pro-inflammatory caspases and reduced IL-1beta staining in the orbito-frontal cortex astrocytes in SNI mice. 
These preliminary data show that peripheral neuropathy induced over-expression of pro-inflammatory/pro-apoptotic caspases in the orbito-frontal cortex and that ozone, by mechanisms that are as yet unknown, can regulate the expression of the genes that play a pivotal role in the onset and maintenance of allodynia.
Quelle:Pubmed (PMID: 19100257): Eur J Pharmacol. 2009 Jan 28;603(1-3):42-9. Epub 2008 Dec 6
Fuccio C, Luongo C, Capodanno P, Giordano C, Scafuro MA, Siniscalco D, Lettieri B, Rossi F, Maione S, Berrino L.
Department of Experimental Medicine, Faculty of Medicine and Surgery, Second University of Naples, Naples, Italy


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Inflammation, Apr 2007:
Ozonotherapy in an induced septic shock.  
Effect of ozonotherapy on rat organs in evaluation of free radical reactions and selected enzymatic systems:
http://www.springerlink.com/content/t55u9272n8248134/

Madej P, Plewka A, Madej JA, Nowak M, Plewka D, Franik G, Golka D
Inflammation Apr 2007; 30(1-2) :52-8
Department and Clinic of Gynaecological Endocrinology, Medical University of Silesia, ul. Medyków 14, 40-752 Katowice, Poland. pmadej@slam.katowice.pl
Zusammenfassung
The confirmed advantageous effects of oxygen/ozone therapy in several clinical conditions stimulated experimental studies on effects of the therapy in rats with an induced septic shock. The studies were conducted on adult male rats of Wistar strain. Four groups of the animals, each of 15 rats, included: I--control group, (C); II--animals intraperitoneally administered with O(2)/O(3) (CO), III--rats given of Escherichia coli endotoxin (lipopolysaccharide-LPS) (CL), IV--rats administered with the lipopolysaccharide plus administered with the oxygen/ozone mixture (OL). Activities of catalase and superoxide dismutase and of free radical reactions were estimated. The exposure to LPS augmented activities of SOD and of catalase in liver, lungs and heart. In all the examined organs LPS induced significant changes in levels of free radicals. 
Except of the lungs, parallel administration of the rats with LPS and ozone/oxygen revoked development of the alterations.
 The obtained results point to a strong, stabilizing and regenerative effect of ozonotherapy.

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Ozone Therapy on Cerebral Blood Flow: A Preliminary Report
Bernardino Clavo, Luis Catalá, Juan L. Pérez, Victor Rodríguez and Francisco Robaina. Siehe folgenden Link:
http://ecam.oxfordjournals.org/cgi/content/full/1/3/315#TBL1
Abstract
Ozone therapy is currently being used in the treatment of ischemic disorders, but the underlying mechanisms that result in successful treatment are not well known. This study assesses the effect of ozone therapy on the blood flow in the middle cerebral and common carotid arteries. 

Seven subjects were recruited for the therapy that was performed by transfusing ozone-enriched autologous blood on 3 alternate days over 1 week. Blood flow quantification in the common carotid artery (n = 14) was performed using color Doppler. Systolic and diastolic velocities in the middle cerebral artery (n = 14) were estimated using transcranial Doppler. Ultrasound assessments were conducted at the following three time points: 1) basal (before ozone therapy), 2) after session #3 and 3) 1 week after session #3. The common carotid blood flow had increased by 75% in relation to the baseline after session #3 (P < 0.001) and by 29% 1 week later (P = 0.039). In the middle cerebral artery, the systolic velocity had increased by 22% after session #3 (P = 0.001) and by 15% 1 week later (P = 0.035), whereas the diastolic velocity had increased by 33% after session #3 (P < 0.001) and by 18% 1 week later (P = 0.023). 
This preliminary Doppler study supports the clinical experience of achieving improvement by using ozone therapy in peripheral ischemic syndromes. Its potential use as a complementary treatment in cerebral low perfusion syndromes merits further clinical evaluation.

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Neroscience Research 41 (2001) 233-241:
Time course of oxidative damage in different brain regions following 
transient cerebral ischemia 
in gerbils 
(Keywords: Oxidative sgtress; Cerebral ischemia; Glutathione; Lipid peroxidation; Antioxidants; Brain.)
 „Reflow to previous ischemic brain results in an increase in oxygen level and consequently causes severe oxidative injury to the tissue by massive production of ROS....“; 4.4. Concluding remarks: „...These results may have important implications for the andioxidant therapy in transient global cerebral ischemia due to the maximal appaerance of reactive oxygen species in the late stages, which suggest that postischemic administration of antioxidants would be probably valuable in preventing hippocampal neuronal loss....“
  http://www.geocities.com/candelariojalil/Neurosci_Res_Candelario-Jalil_et_al_2001.pdf

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JOURNAL OF ALZHEIMER'S DISEASE, October 2009
Increasing evidence of oxidative stress in patients with Alzheimer’s disease

http://www.j-alz.com/issues/18/vol18-2.html
JOURNAL OF ALZHEIMER'S DISEASE Volume 18, Number 2, October 2009, Pages 345-353
Pei-Ning Wang, Hsin-Chen Lee, Chun-Hui Wang, Yueh-Hsin Ping, Tsung-Yun Liu, Chin-Wen Chi, Ker-Nen Lin, Hsu-Chih Liu 
Heteroplasmy of Mitochondrial D310 Mononucleotide Repeat Region in the Blood of Patients with Alzheimer’s Disease
Abstract: There is increasing evidence of oxidative stress in patients with Alzheimer’s disease (AD) and mild cognitive impairment (MCI). Because mitochondrial DNA (mtDNA) is susceptible to oxidative damage, somatic mtDNA mutations may be induced by oxidative stress.

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Ozone Biological Response in Kidneys of Rats Submitted to Warm Ischemia 
in: Ozone Science & Engineering, Vol 25; 233-240 (2003)

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Mediators Inflamm. 2005; 2005(4): 221–227 
Ozone Therapy on Rats Submitted to Subtotal Nephrectomy: Role of Antioxidant System 
siehe: http://www.pubmedcentral.gov/articlerender.fcgi?artid=1526476
Zitat:  „Taking into account some of the ozone therapeutic properties, such as antiplatelet activity, enhancement of cell energy, and the increase of the antioxidant defense system, the aim of this paper is to evaluate the effect of ozone therapy in the renal function, morphology, and biochemical parameters that measure oxidative stress in an experimental model of CRF.“ (chronic renal failure)

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Mediators of Inflammation, 1998
Ozone oxidative preconditioning: 
Protection against cellular damage by free radicals. 
Die hepatotoxische Wirkung von Tertrachlorkohlenstoff kann durch Vorbehandlung der Versuchstiere mit rectalen Ozonapplikationen drastisch vermindert werden.
publiziert in: Mediators of Inflammation, 7, 289–294 (1998)
siehe: Leon_Ozone_ox_Precond_CCL4.pdf
by O.S. Leon, S. Menendez, N. Merino, R.Castillo, S. Sam, L.Perez, E. Cruz and V. Bocci ( Center for Research and Biological Evaluation Havana and Ozone research Center Havana andNational Center for Schientific Research and Institute of General Physiology, University of Siena, Italy:

„To our knowledge these are the first 
experimental results showing that repeated administration of ozone in atoxic doses is able to induce an adaptation to oxidative stress thus 
enabling the animals to maintain hepatocellular integrity after CCl4 poisoning...“ 

Abstract:
THERE is some anecdotal evidence that oxygen-ozone therapy may be beneficial in some human diseases. 
However so far only a few biochemical and pharmacodynamic mechanisms have been elucidated. 
On the basis of preliminary data we postulated that controlled ozone administration would promote an oxidative preconditioning preventing the hepatocellular damage mediated by free radicals. 

Six groups of rats were classified as follows: 
(1) negative control, using intraperitoneal sunflower oil; 
(2) positive control using carbon tetrachloride (CCl4) as an oxidative 
        challenge; 
(3) oxygen-ozone, pretreatment via rectal insufflation (15 sessions) and 
        after it,  CCl4; 
(4) oxygen, as group 3 but using oxygen only; 
(5) control oxygen-ozone, as group 3, but without CCl4; group 
(6) control oxygen, as group 5, but using oxygen only. 


We have evaluated critical biochemical parameters such as levels of transaminase, cholinesterase, superoxide dismutase, catalase, phospholipase A, calcium 
dependent ATPase, reduced glutathione, glucose 6 phosphate dehydrogenase and lipid peroxidation. 

Interestingly, in spite of CCl4 - Administration, group 3 did not differ from group 1, while groups 2 and 4 showed significant differences from groups 1 and 3 and displayed hepatic damage. 

Key words: Ozone, Oxidative stress, Preconditioning, Free 
radicals, Antioxidant defence system 
Mediators of Inflammation, 7, 289–294 (1998)


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The Journal of Biological Chemistry;  Nov 25, 2005

Krebs (Ovarial-/ Colon-Ca) und Mg-Superoxiddismutase/Oxidativer Stress:
 
„Our findings suggest that the increase in Mn-SOD expression in ovarian cancer is a cellular response to intrinsic ROS stress and that scavenging of superoxide by SOD may alleviate the ROS stress and thus reduce the stimulating effect of ROS on cell growth. Suppression of Mn-SOD expression caused accumulation of ROS, leading to increased cell proliferation in vitro an rapid tumor growth in vivo.“
 (The Journal of Biological Chemistry Vol 280,No 47, pp 39485-39492, Nov 25, 2005 bzw. Molecular and Cellular Biology Sept.2005)
http://www.jbc.org/cgi/reprint/280/47/39485  und  
 http://mcb.asm.org/cgi/reprint/25/17/7758


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Changes in leukocyte population after ozonated autohemoadministration in cows with inflammatory diseases.
Ohtsuka H, Ogata A, Terasaki N, Koiwa M, Kawamura S
J Vet Med Sci Feb 2006; 68(2) :175-8
Volltext kostenfrei beim Verlag erhältlich 
Department of Large Animal Internal Medicine, School of Veterinary Medicine and Animal Sciences, Kitasato University, Towada, Aomori 034-8628, Japan.
Abstract
In this study, we investigated whether ozonated autohemoadministration (OAHA) influences leukocyte populations in cows with clinical inflammatory disease. Eleven cows with inflammatory disease (Inflammatory Group) and three healthy cows (Control Group) were used for this study. The CD4(+)/CD8(+) ratio in the Inflammatory Group increased significantly compared to that in the Control Group 3 to 4 days after OAHA treatment. In the Inflammatory Group, the number of CD14(+) cells decreased gradually after OAHA, but CD14(+) levels remained stable in the Control Group. The number of MHC class-II(+) cells decreased gradually in the Inflammatory Group, but increased gradually in the Control Group, and the difference between the groups was significant on day 14 after OAHA. These findings suggest a possible difference in the activation of immune response after OAHA in infected cows compared to healthy cows.

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h/medical_and_more/Search_Results?ACTION=AUTHOR&author=Franik+Ghttp://www.univadis.ch/medical_and_more/Search_Results?ACTION=AUTHOR&author=Golka+Dmailto:pmadej@slam.katowice.plhttp://ecam.oxfordjournals.org/cgi/content/full/1/3/315#TBL1http://www.geocities.com/candelariojalil/Neurosci_Res_Candelario-Jalil_et_al_2001.pdfhttp://www.pubmedcentral.gov/articlerender.fcgi?artid=1526476Forschung_files/Leon_Ozone_ox_Precond_CCL4.pdfhttp://www.jbc.org/cgi/reprint/280/47/39485http://mcb.asm.org/cgi/reprint/25/17/7758http://www.univadis.ch/medical_and_more/Search_Results?ACTION=AUTHOR&author=Ohtsuka+Hhttp://www.univadis.ch/medical_and_more/Search_Results?ACTION=AUTHOR&author=Ogata+Ahttp://www.univadis.ch/medical_and_more/Search_Results?ACTION=AUTHOR&author=Terasaki+Nhttp://www.univadis.ch/medical_and_more/Search_Results?ACTION=AUTHOR&author=Koiwa+Mhttp://www.univadis.ch/medical_and_more/Search_Results?ACTION=AUTHOR&author=Kawamura+Shttp://joi.jlc.jst.go.jp/JST.JSTAGE/jvms/68.175?from=PubMedKlinische_Studien.htmlshapeimage_1_link_0shapeimage_1_link_1shapeimage_1_link_2shapeimage_1_link_3shapeimage_1_link_4shapeimage_1_link_5shapeimage_1_link_6shapeimage_1_link_7shapeimage_1_link_8shapeimage_1_link_9shapeimage_1_link_10shapeimage_1_link_11shapeimage_1_link_12shapeimage_1_link_13shapeimage_1_link_14shapeimage_1_link_15shapeimage_1_link_16shapeimage_1_link_17shapeimage_1_link_18shapeimage_1_link_19shapeimage_1_link_20shapeimage_1_link_21shapeimage_1_link_22shapeimage_1_link_23shapeimage_1_link_24shapeimage_1_link_25shapeimage_1_link_26shapeimage_1_link_27shapeimage_1_link_28shapeimage_1_link_29shapeimage_1_link_30shapeimage_1_link_31shapeimage_1_link_32shapeimage_1_link_33shapeimage_1_link_34shapeimage_1_link_35shapeimage_1_link_36shapeimage_1_link_37shapeimage_1_link_38shapeimage_1_link_39shapeimage_1_link_40shapeimage_1_link_41shapeimage_1_link_42shapeimage_1_link_43shapeimage_1_link_44shapeimage_1_link_45shapeimage_1_link_46
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