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Статті в журналах з теми "Mime de Superoxyde Dismutase (SOD)"
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Gumay, Ainun Rahmasari, Saekhol Bakri, and Astika Widy Utomo. "The Effect of Green Tea Leaf Extract on Spatial Memory Function and Superoxyde Dismutase Enzyme Activity in Mice with D-galactose Induced Dimentia." Sains Medika 8, no. 1 (April 4, 2017): 8. http://dx.doi.org/10.26532/sainsmed.v8i1.1050.
Повний текст джерелаАнотація:
Background:�Oxidative stress�and�inflammation�play�an important role in�pathogenesis of�brain aging�and neurodegenerative diseases such as�Alzheimer. Green tea�has been shown to have antioxidant, anti-inflammatory, anticancer, and neuroprotective�activity. Objectives: to determine the effect of green tea extract on�spatial memory function and superoxide dismutase�enzyme activity in mice with D-galactose induced dementiaMethods:�An experimental study using "post test only control group design".�Twenty male�BALB/c Mice aged 6-8�weeks were divided into�4�groups.�Negative control group�(NG)�was induced by subcutaneous injection of�D-galactose�(150�mg/kg BW)�once�daily for�6�weeks.�GT-90, GT-270,�GT-540�were induced by�D-galactose�and orally administered with 90, 270, and 540 mg/kg BW of�green tea extract�once daily for 6 weeks.�The spatial memory functions were assessed using Morris water maze and�SOD enzyme activities�were evaluated using ELISA.�One-way Anova and Kruskal-Wallis were used for statistical analysis.�Results: mean�percentage of latency time in the GT-90�(35.29�(SD=�2.69)%),�GT-270�(35.28 (SD= 2.62)%), and�GT-540�(35.62�(SD=5.05)%)�were�significantly�higher compared to that of NG�(20.38�(SD =�3.21)%), p�<0.05). SOD enzyme activity in the�GT-270�(0.78 (SD = 0.07) U/ml)�was�significantly�higher�compared to that of NG�(0.51 (SD = 0.01) U�ml), p= 0.004).Conclusion:�Green tea extract�may�improve�spatial memory�function�and�the activity of�superoxide dismutase�enzyme in mice�with D-galactose induced�dementia.
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Marufah, Marufah, and M. Adib. "EKSTRAK BUAH PEPAYA (Carica papaya L.) MENINGKATKAN KADAR CATALASE DAN GLUTATHIONE HATI TIKUS YANG TERPAPARLEAD ACETATE." Jurnal SainHealth 2, no. 1 (March 28, 2018): 8. http://dx.doi.org/10.51804/jsh.v2i1.170.8-12.
Повний текст джерелаАнотація:
Pollution is an entry or inclusion living things, subtances, energy, and or other components into environment and or change of environment compositions because of human activity or natural process with the result that decrease of quality to certain level that causes doesn’t work environment. Pollution can be caused many subtances that is heavy metal, i.e. lead acetate (Pb). Lead acetate affect physiological aberration, biochemical, and behavior. Heavy metal induction induce ROS production act as destructive oxidants. Body capability to oxidant neutralize serviced by superoxyde dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), glutathione (GSH), vitamin C, vitamin E, and other antioxidants in the cell. Antioxidants synthesized by plants, which is papaya (Carica papaya L.). Papaya (Carica papaya L.) effect on CAT and GSH levels was performed on male mice wistar strain. Mice induced by lead acetate 20 gr / Kg weight dose for 6 weeks, given papaya extract 100, 200, and 400 mg/Kg weight dose for 6 weeks. Further glutathione and catalase levels are measured on mice liver. This study proves, papaya extract increase catalase levels (p = 0,000) and glutathione levels (p = 0,000) on mice liver induced lead acetate. Papaya extract 400 mg/Kg/day most effective dose to increase catalase and glutathione levels on mice liver induced lead acetate.
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Curti, Valeria, Vincenzo Zaccaria, Arold Tsetegho Sokeng, Marco Dacrema, Irene Masiello, Anna Mascaro, Giuseppe D’Antona, and Maria Daglia. "Bioavailability and In Vivo Antioxidant Activity of a Standardized Polyphenol Mixture Extracted from Brown Propolis." International Journal of Molecular Sciences 20, no. 5 (March 12, 2019): 1250. http://dx.doi.org/10.3390/ijms20051250.
Повний текст джерелаАнотація:
Several lines of evidence demonstrate the antioxidant, anti-inflammatory and antimicrobial activities of propolis, mostly ascribed to its polyphenol content. However, little is known regarding the bioavailability of propolis in acute and prolonged settings of oral administration. In this study, we first determined the content of the main polyphenols in a brown propolis extract obtained using a patented extraction method (Multi Dinamic Extraction—M.E.D.) by RP-HPLC-UV-PDA-MSn analysis, followed by the bioavailability of galangin and chrysin, the most abundant polyphenols in the mixture (7.8% and 7.5% respectively), following acute (single bolus of 500 mg/kg containing about 3.65 mg of the polyphenol mixture) and prolonged (100, 250 and 500 mg/kg body for 30 days) oral administration in 30 male 8 weeks old C57BL/6 wild-type mice. In the acute setting, blood was taken at 30 s and 5, 10, 15, 20, 25, 30, 45, 60 and 120 min following the oral bolus. In the prolonged setting, blood samples were obtained after 10, 20 or 30 days of administration. At the end of treatment, expression of antioxidant enzymes (superoxyde dismutase, SOD-1; catalase, CAT; glutathione peroxidase, GSS) was evaluated in liver tissue. Following both acute and prolonged administration, neither galangin nor chrysin were detectable in the plasma of mice, whereas the glucuronide metabolite of galangine was detectable 5 min after acute administration. At the end of the prolonged treatment SOD-1 was found to have increased significantly, unlike CAT and GSS. Overall, these data suggest that oral administration of whole brown propolis extract is followed by rapid absorption and metabolization of galangin followed by adaptations of the antioxidant first line defense system.
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BROWN, David R., and Andreas BESINGER. "Prion protein expression and superoxide dismutase activity." Biochemical Journal 334, no. 2 (September 1, 1998): 423–29. http://dx.doi.org/10.1042/bj3340423.
Повний текст джерелаАнотація:
The function of the prion protein (PrPc) remains uncertain. It has been suggested that prion protein expression may aid cellular resistance to oxidative stress by influencing the activity of Cu/Zn superoxide dismutase (Cu,Zn SOD). The activity of Cu,Zn SOD was investigated in mice with different levels of PrPc expression. Increasing levels of PrPc expression were linked to increased levels of Cu,Zn SOD activity. Western-blot and Northern-blot analysis indicated that mice either lacking or overexpressing PrPc had levels of Cu,Zn SOD mRNA equivalent to those expressed in wild-type mice. Mice overexpressing the prion protein had lower levels of resistance to oxidative stress but higher expression levels of glutathione peroxidase, probably due to increased levels of hydrogen peroxide produced by increased Cu,Zn SOD activity. When cells were metabolically labelled with radioactive copper, increased radioactivity was immunoprecipitated with Cu,Zn SOD from mice with higher levels of PrPc. In addition, diethyldithiocarbamate, a copper chelator that inactivates Cu,Zn SOD by capturing copper from the molecule, is more able to inactivate Cu,Zn SOD expressed in animals with higher levels of PrPc. As recent studies have suggested that PrPc may regulate some aspect of copper metabolism, it is suggested that PrPc expression may regulate Cu,Zn SOD activity by influencing copper incorporation into the molecule.
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Carvalho-Queiroz, Claudia, Rosemary Cook, Ching C. Wang, Rodrigo Correa-Oliveira, Nicola A. Bailey, Nejat K. Egilmez, Edith Mathiowitz, and Philip T. LoVerde. "Cross-Reactivity of Schistosoma mansoni Cytosolic Superoxide Dismutase, a Protective Vaccine Candidate, with Host Superoxide Dismutase and Identification of Parasite-Specific B Epitopes." Infection and Immunity 72, no. 5 (May 2004): 2635–47. http://dx.doi.org/10.1128/iai.72.5.2635-2647.2004.
Повний текст джерелаАнотація:
ABSTRACT Schistosoma mansoni, an intravascular parasite, has evolved a number of immune evasion mechanisms to establish itself in the host, such as antioxidant enzymes. Our laboratory has demonstrated that the highest levels of certain antioxidant enzymes are found in adult worms, which are the least susceptible to immune killing. Vaccination of mice with naked DNA constructs containing the gene encoding Cu/Zn cytosolic superoxide dismutase (SmCT-SOD) showed significant levels of protection compared to a control group, and our data demonstrate that the adult worms are a target of the immune response that confers resistance in SmCT-SOD DNA-vaccinated mice. Because SmCT-SOD shows significant identity with the human homologue, we evaluated the reactivity of anti-SmCT-SOD antibodies derived from SmCT-SOD-immunized mice and rabbits and from S. mansoni-infected individuals to human superoxide dismutase (hSOD) and SmCT-SOD parasite-specific peptides to assess the potential for autoimmune responses from immunization with the recombinant molecule. In addition, we evaluated the ability of various SmCT-SOD adjuvant-delivered immunizations to induce cross-reactive antibodies. Both mouse and rabbit antibodies generated against SmCT-SOD recognized the denatured form of hSOD. The same antibodies did not recognize nondenatured hSOD. Sera from infected individuals with different clinical forms of schistosomiasis recognized SmCT-SOD but not hSOD. Antibodies from mice immunized with different SmCT-SOD-containing formulations of both DNA and protein were able to recognize SmCT-SOD-derived peptides but not soluble hSOD. All together, these findings serve as a basis for developing a subunit vaccine against schistosomiasis.
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Park, Jong Woong, Wen-Ning Qi, Yongting Cai, Igor Zelko, John Q. Liu, Long-En Chen, James R. Urbaniak, and Rodney J. Folz. "Skeletal muscle reperfusion injury is enhanced in extracellular superoxide dismutase knockout mouse." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 1 (July 2005): H181—H187. http://dx.doi.org/10.1152/ajpheart.00458.2004.
Повний текст джерелаАнотація:
This study investigates the role of extracellular SOD (EC-SOD), the major extracellular antioxidant enzyme, in skeletal muscle ischemia and reperfusion (I/R) injury. Pedicled cremaster muscle flaps from homozygous EC-SOD knockout (EC-SOD−/−) and wild-type (WT) mice were subjected to 4.5-h ischemia and 90-min reperfusion followed by functional and molecular analyses. Our results revealed that EC-SOD−/− mice showed significantly profound I/R injury compared with WT littermates. In particular, there was a delayed and incomplete recovery of arterial spasm and blood flow during reperfusion, and more severe acute inflammatory reaction and muscle damage were noted in EC-SOD−/− mice. After 90-min reperfusion, intracellular SOD [copper- and zinc-containing SOD (CuZn-SOD) and manganese-containing (Mn-SOD)] mRNA levels decreased similarly in both groups. EC-SOD mRNA levels increased in WT mice, whereas EC-SOD mRNA was undetectable, as expected, in EC-SOD−/− mice. In both groups of animals, CuZn-SOD protein levels decreased and Mn-SOD protein levels remained unchanged. EC-SOD protein levels decreased in WT mice. Histological analysis showed diffuse edema and inflammation around muscle fibers, which was more pronounced in EC-SOD−/− mice. In conclusion, our data suggest that EC-SOD plays an important role in the protection from skeletal muscle I/R injury caused by excessive generation of reactive oxygen species.
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Mathias, Maxwell, Joann Taylor, Elizabeth Mendralla, and Marta Perez. "Neonatal Extracellular Superoxide Dismutase Knockout Mice Increase Total Superoxide Dismutase Activity and VEGF Expression after Chronic Hyperoxia." Antioxidants 10, no. 8 (August 1, 2021): 1236. http://dx.doi.org/10.3390/antiox10081236.
Повний текст джерелаАнотація:
Bronchopulmonary dysplasia (BPD) is a common lung disease affecting premature infants that develops after exposure to supplemental oxygen and reactive oxygen intermediates. Extracellular superoxide dismutase (SOD3) is an enzyme that processes superoxide radicals and has been shown to facilitate vascular endothelial growth factor (VEGF) and nitric oxide (NO) signaling in vascular endothelium. We utilized a mouse model of neonatal hyperoxic lung injury and SOD3 knockout (KO) mice to evaluate its function during chronic hyperoxia exposure. Wild-type age-matched neonatal C57Bl/6 (WT) and SOD3−/− (KO) mice were placed in normoxia (21% FiO2, RA) or chronic hyperoxia (75% FiO2, O2) within 24 h of birth for 14 days continuously and then euthanized. Lungs were harvested for histologic evaluation, as well as comparison of antioxidant enzyme expression, SOD activity, VEGF expression, and portions of the NO signaling pathway. Surprisingly, KO-O2 mice survived without additional alveolar simplification, microvascular remodeling, or nuclear oxidation when compared to WT-O2 mice. KO-O2 mice had increased total SOD activity and increased VEGF expression when compared to WT-O2 mice. No genotype differences were noted in intracellular antioxidant enzyme expression or the NO signaling pathway. These results demonstrate that SOD3 KO mice can survive prolonged hyperoxia without exacerbation of alveolar or vascular phenotype.
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Dirami, Ghenima, Donald Massaro, and Linda Biadasz Clerch. "Regulation of lung manganese superoxide dismutase: species variation in response to lipopolysaccharide." American Journal of Physiology-Lung Cellular and Molecular Physiology 276, no. 5 (May 1, 1999): L705—L708. http://dx.doi.org/10.1152/ajplung.1999.276.5.l705.
Повний текст джерелаАнотація:
Lipopolysaccharide (LPS) treatment increases survival of rats, but not of mice, during hyperoxia. Manganese superoxide dismutase (Mn SOD) in the lung plays a critical role in LPS-induced tolerance to hyperoxia in rats. Therefore, we now compared the response of lung Mn SOD with treatment of mice and rats with LPS. LPS treatment of rats increased Mn SOD activity and protein concentration, did not change its specific activity, increased Mn SOD mRNA concentration 35-fold, and elevated Mn SOD synthesis 50% without changing general protein synthesis. LPS treatment of mice did not alter any of these parameters except for a 16-fold increase in Mn SOD mRNA concentration. Mn SOD translational efficiency (synthesis/mRNA concentration) was diminished 93% in rat lung and 76% in mouse lung by treatment with LPS. However, the absolute translational efficiency was twofold higher in lungs of LPS-treated rats than in lungs of LPS-treated mice. The failure of LPS to raise Mn SOD activity in mouse lungs is due, at least in part, to a smaller increase in Mn SOD mRNA and lower translational efficiency in LPS-treated mice than in LPS-treated rats.
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Ookawara, Tomomi, Nobuo Imazeki, Osamu Matsubara, Takako Kizaki, Shuji Oh-Ishi, Chitose Nakao, Yuzo Sato, and Hideki Ohno. "Tissue distribution of immunoreactive mouse extracellular superoxide dismutase." American Journal of Physiology-Cell Physiology 275, no. 3 (September 1, 1998): C840—C847. http://dx.doi.org/10.1152/ajpcell.1998.275.3.c840.
Повний текст джерелаАнотація:
Protein content and mRNA expression of extracellular superoxide dismutase (EC-SOD) were investigated in 16 mouse tissues. We developed a double-antibody sandwich ELISA using the affinity-purified IgG against native mouse EC-SOD. EC-SOD could be detected in all of the tissues examined (lung, kidney, testis, brown fat, liver, adrenal gland, pancreas, colon, white fat, thymus, stomach, spleen, heart, skeletal muscle, ileum, and brain, in decreasing order of content measured as μg/g wet tissue). Lung showed a markedly higher value of EC-SOD than other tissues. Interestingly, white fat had a high content of EC-SOD in terms of micrograms per milligram protein, which corresponded to that of lung. Kidney showed the strongest expression of EC-SOD mRNA. Relatively strong expression of the mRNA was observed in lung, white fat, adrenal gland, brown fat, and testis. Heart and brain showed only weak signals, and no such expression could be detected in either digestive organs or skeletal muscle. Immunohistochemically, EC-SOD was localized mainly to connective tissues and vascular walls in the tissues examined. Deep staining in the cytosol was observed in the cortical tubular cells of kidney. These results suggest that EC-SOD is distributed systemically in mice and that the physiological importance of this enzyme may be a compensatory adaptation to oxidative stress, particularly in lung and kidney.
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Bowler, Russell P., Mike Nicks, Karrie Warnick, and James D. Crapo. "Role of extracellular superoxide dismutase in bleomycin-induced pulmonary fibrosis." American Journal of Physiology-Lung Cellular and Molecular Physiology 282, no. 4 (April 1, 2002): L719—L726. http://dx.doi.org/10.1152/ajplung.00058.2001.
Повний текст джерелаАнотація:
Bleomycin administration results in well-described intracellular oxidative stress that can lead to pulmonary fibrosis. The role of alveolar interstitial antioxidants in this model is unknown. Extracellular superoxide dismutase (EC-SOD) is the primary endogenous extracellular antioxidant enzyme and is abundant in the lung. We hypothesized that EC-SOD plays an important role in attenuating bleomycin-induced lung injury. Two weeks after intratracheal bleomycin administration, we found that wild-type mice induced a 106 ± 25% increase in lung EC-SOD. Immunohistochemical staining revealed that a large increase in EC-SOD occurred in injured lung. Using mice that overexpress EC-SOD specifically in the lung, we found a 53 ± 14% reduction in bleomycin-induced lung injury assessed histologically and a 17 ± 6% reduction in lung collagen content 2 wk after bleomycin administration. We conclude that EC-SOD plays an important role in reducing the magnitude of lung injury from extracellular free radicals after bleomycin administration.
Дисертації з теми "Mime de Superoxyde Dismutase (SOD)"
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Mathieu, Émilie. "Anti-oxidant Mn(II)-complexes : design and study in a cellular model of inflammatory diseases. Investigation of subcellular location." Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066428.
Повний текст джерелаАнотація:
Les espèces réactives de l'oxygène (ROS) sont produites en continu dans tous les organismes aérobies et sont impliquées dans la signalisation cellulaire, les défenses contre les pathogènes, mais aussi le stress oxydant. Ce dernier correspond à un déséquilibre entre la production des ROS et leur prise en charge par les défenses anti-oxydantes de la cellule. Le stress oxydant est associé à de nombreuses pathologies, notamment les maladies inflammatoires chroniques de l'intestin (MICI). Parmi les métallo-enzymes qui contrôlent la concentration en ROS, les superoxide dismutases (SOD) jouent un rôle essentiel. Ces enzymes sont responsables de la régulation du superoxyde le premier ROS produit lors de la réduction du dioxygène. Dans ces travaux, des complexes de Mn(II) mimant l'activité de la Mn-SOD (SODm) ont été conçus en utilisant une approche biomimétique. Leur intérêt pour limiter le stress oxydant et l'inflammation dans un modèle cellulaire des MICI a été examiné. En particulier, leur activité biologique a été étudiée au vu de leurs propriétés physico-chimiques et de leur biodisponibilité. Les résultats obtenus avec un complexe parent ont mené à la conception d'une deuxième génération de SODm couplés à une sonde multimodale, à des peptides pénétrants, ou à des peptides adressant aux mitochondries. L'étude du complexe parent fonctionnalisé par des peptides polyarginines a démontré l'influence de charges positives portées par le ligand sur la constante de vitesse. Dans la continuité de l'approche biomimétique développée ici, la conception de SODm de novo est présentée et constitue un premier pas vers l'imitation de l'influence de la seconde sphère de coordinationReactive oxygen species (ROS) are produced continuously in all aerobic organisms and are involved in cell signaling, defenses against pathogens, but also oxidative stress. This latter corresponds to an imbalance between ROS production and their consumption by the antioxidant defenses of the cell. Oxidative stress is associated with numerous pathologies, such as inflammatory bowel diseases (IBD). Among the metalloenzymes controlling the concentration of ROS, superoxide dismutases (SOD) play a crucial role. These enzymes are responsibles for the regulation of superoxide, the first ROS produced by the reduction of oxygen. In this work, Mn(II) complexes mimicking the activity of the Mn-SOD (SODm) were designed using a biomimetic approach. Their relevance to limit oxidative stress and inflammation in a cellular model of IBD was investigated. In particular, their biological activity was studied in light of their physico-chemical properties and of their bioavailability. The results obtained with a parent complex led to the design of a second generation of SOD mimics conjugated with a single core multimodal probe, cell-penetrating peptides, or mitochondria-penetrating peptides. An effect of electrostatic interactions on the catalytic rate constant of the parent complex functionalized with polyarginines peptides was demonstrated, similarly to what is observed for the enzyme. In the continuity of the biomimetic approach envisioned here, the design of de novo SOD mimics is presented and constitutes a first step toward the mimicry of second sphere influence
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Zoumpoulaki, Martha. "MnSOD Mimics : analytical mass spectrometry-based techniques to quantify their amount and biological effect in inflamed intestinal epithelial cells." Thesis, Sorbonne université, 2021. http://www.theses.fr/2021SORUS518.
Повний текст джерелаАнотація:
Le déséquilibre intracellulaire entre antioxydants et pro-oxydants est impliqué dans le développement de nombreuses pathologies, comme les maladies inflammatoires chroniques intestinales-MICI. Le fait que la superoxyde dismutase à manganèse (MnSOD) soit la première ligne de défense antioxydante nous a conduit à tester le rôle des mimes de SOD comme agents anti-inflammatoire dans le contexte des MICI. Mn1 est facilement synthétisé, stable, avec une bonne activité anti-superoxyde intrinsèque et anti-inflammatoire sur des cellules épithéliales intestinales (HT29-MD2) en situation de stress oxydant. La présence de Mn1 intact (ligand+Mn2+) à l'intérieur des HT29-MD2, créées pour étudier l'inflammation intestinale est démontrée avec une stratégie en spectrométrie de masse (IMS-MS). Après 6 h d'incubation avec 100 µM Mn1 et LPS 0.1 µg/mL, Mn1 a été détecté en forme intacte avec une concentration intracellulaire estimée à 10 µM. En utilisant la stratégie OcSILAC, qui permet de quantifier simultanément l’expression des protéines et le niveau d’oxydation de cystéines de l’ensemble du protéome, nous avons démontré qu’une oxydation est induite par le LPS dès 15min (dans la fraction organelles dont la mitochondrie) et qu’elle se résout après 6h-LPS, avec une surexpression de la MnSOD (dès 3h). Quand il est coincubé avec LPS, Mn1 est capable de limiter l’oxydation totale des protéines à 15 min (70% dans les membranes/organelles) et de remplacer l’action de la MnSOD à 6h. Mn1 également rétablit en leur niveau basal la majorité des protéines sous et surexprimées par l’activation au LPS. Nos résultats démontrent ainsi le potentiel du Mn1 comme nouvel agent thérapeutique contre les MICIThe intracellular imbalance between antioxidants and pro-oxidants is involved in the development of many pathologies (like chronic inflammatory bowel diseases-IBD). The fact that manganese superoxide dismutase (MnSOD) is the first line of antioxidant defense led us to study the role of MnSOD mimics as anti-inflammatory agents in the context of IBD. Mn1 is easily synthesized, stable, with good intrinsic anti-superoxide activity and anti-inflammatory activity on intestinal epithelial cells (HT29-MD2). The presence of intact Mn1 (ligand+Mn2+) inside HT29-MD2, created to study intestinal inflammation, was demonstrated using mass spectrometry (IMSMS). After 6h of incubation with 100 µM Mn1 and with LPS 0.1 µg/mL, Mn1 was detected intact with an estimated intracellular concentration of 10 µM. Using the OcSILAC strategy, making possible to simultaneously quantify protein expression and oxidation at the proteome-wide cysteine level, it has been demonstrated that an oxidation was induced by LPS from 15min (in the organelles fraction, including mitochondria) and was resolved after 6h-LPS, with an overexpression of MnSOD (after 3h). When coincubated with LPS, Mn1 limited the total protein oxidation at 15min (70% in the membranes/organelles) and compensate for MnSOD at 6h. Mn1 also restored to their basal levels most of the proteins that were under and overexpressed upon LPS activation. Our results thus demonstrate the potential of Mn1 as a new therapeutic agent against IBD
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Roy, Monica. "Étude des superoxyde dismutases (SOD) dans l'oviducte bovin." Thesis, Université Laval, 2008. http://www.theses.ulaval.ca/2008/25279/25279.pdf.
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Olofsson, Eva. "Superoxide dismutase 1 and cataract." Doctoral thesis, Umeå : Umeå universitet, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-21032.
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Zetterström, Per. "Misfolded superoxide dismutase-1 in amyotrophic lateral sclerosis." Doctoral thesis, Umeå universitet, Klinisk kemi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-43898.
Повний текст джерелаАнотація:
Amyotrophic lateral sclerosis (ALS) is a disease in which the motor neurons die in a progressive manner, leading to paralysis and muscle wasting. ALS is always fatal, usually through respiratory failure when the disease reaches muscles needed for breathing. Most cases are sporadic, but approximately 5–10% are familial. The first gene to be linked to familial ALS encodes the antioxidant enzyme superoxide dismutase-1 (SOD1). Today, more than 160 different mutations in SOD1 have been found in ALS patients. The mutant SOD1 proteins cause ALS by gain of a toxic property that should be common to all. Aggregates of SOD1 in motor neurons are hallmarks of ALS patients and transgenic models carrying mutant SOD1s, suggesting that misfolding, oligomerization, and aggregation of the protein may be involved in the pathogenesis. SOD1 is normally a very stable enzyme, but the structure has several components that make SOD1 sensitive to misfolding. The aim of the work in this thesis was to study misfolded SOD1 in vivo. Small amounts of soluble misfolded SOD1 were identified as a common denominator in transgenic ALS models expressing widely different forms of mutant SOD1, as well as wild-type SOD1. The highest levels of misfolded SOD1 were found in the vulnerable spinal cord. The amounts of misfolded SOD1 were similar in all the different models and showed a broad correlation with the lifespan of the different mouse strains. The misfolded SOD1 lacked the C57-C146 intrasubunit disulfide bond and the stabilizing zinc and copper ions, and was prinsipally monomeric. Forms with higher apparent molecular weights were also found, some of which might be oligomers. Misfolding-prone monomeric SOD1 appeared to be the principal source of misfolded SOD1 in the CNS. Misfolded SOD1 in the spinal cord was found to interact mainly with chaperones, with Hsc70 being the most important. Only a minor proportion of the Hsc70 was sequestered by SOD1, however, suggesting that chaperone depletion is not involved in ALS. SOD1 is normally found in the cytoplasm but can be secreted. Extracellular mutant SOD1 has been found to be toxic to motor neurons and glial cells. Misfolded SOD1 in the extracellular space could be involved in the spread of the disease between different areas of the CNS and activate glial cells known to be important in ALS. The best way to study the interstitium of the CNS is through the cerebrospinal fluid (CSF), 30% of which is derived from the interstitial fluid. Antibodies specific for misfolded SOD1 were used to probe CSF from ALS patients and controls for misfolded SOD1. We did find misfolded SOD1 in CSF, but at very low levels, and there was no difference between ALS patients and controls. This argues against there being a direct toxic effect of extracellular SOD1 in ALS pathogenesis. In conclusion, soluble misfolded SOD1 is a common denominator for transgenic ALS model mice expressing widely different mutant SOD1 proteins. The misfolded SOD1 is mainly monomeric, but also bound to chaperones, and possibly exists in oligomeric forms also. Misfolded SOD1 in the interstitium might promote spread of aggregation and activate glial cells, but it is too scarce to directly cause cytotoxicity.
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Jonsson, P. Andreas. "Superoxide dismutase 1 and amyotrophic lateral sclerosis." Doctoral thesis, Umeå : Medical Biosciences, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-611.
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Bergemalm, Daniel. "Mutant superoxide dismutase-1-caused pathogenesis in amyotrophic lateral sclerosis." Doctoral thesis, Umeå : Umeå university, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-31116.
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Kattan, Zilal. "Rôle de la superoxyde dismutase à manganèse et de la protéine damaged DNA binding 2 dans la croissance tumorale mammaire." Thesis, Nancy 1, 2009. http://www.theses.fr/2009NAN10040/document.
Повний текст джерелаАнотація:
Récemment, notre laboratoire a démontré pour la première fois, que la protéine Damaged DNA Binding 2 (DDB2) possédait une activité régulatrice négative de l’expression basale de la superoxyde dismutase mitochondriale (SOD Mn) en se fixant sur un élément de réponse dans la région promotrice de son gène. Cette protéine était connue jusque là pour sa participation dans le système de réparation de l’ADN par excision de nucléotides. L’objectif de ce travail a été de définir précisément l’implication de ces deux protéines dans la croissance des cellules d’adénocarcinome mammaire, en développant des modèles cellulaires dont l’expression de la SOD Mn ou de la DDB2 est modulée expérimentalement. Nos résultats montrent pour la 1ère fois, que la SOD Mn est surexprimée dans les cellules tumorales mammaires insensibles aux oestrogènes (ER-) et ayant un pouvoir métastatique, et non dans les cellules épithéliales mammaires normales et les cellules ER+. L’inhibition de l’expression de la SOD Mn entraîne une stimulation de la croissance et une diminution de l’invasivité cellulaires, associées à une activité réduite de la métalloprotéinase 9. L’addition d’antioxydants, éliminant spécifiquement l’H2O2 issu de l’activité élevée de la SOD Mn, entraîne à la fois une inhibition de la croissance et du pouvoir invasif des cellules ER-. Ces résultats révèlent que la SOD Mn participe aux capacités invasives des cellules ER- via la production d’H2O2. Nous avons également montré pour la 1ère fois, que la DDB2 présente une activité oncogénique dans les cellules tumorales mammaires sensibles aux oestrogènes (ER+), non seulement parce que son gène est surexprimé, mais également parce qu’elle active leur prolifération en agissant sur la phase de transition G1/S et sur la progression dans la phase S du cycle cellulaire. Contrairement à la SOD Mn, l’expression de la DDB2 n’est pas observée dans les cellules tumorales mammaires ER-. De même à partir de biopsies provenant de patientes atteintes d’un cancer du sein, nous avons montré que la DDB2 est significativement plus exprimée dans les tumeurs les moins agressives et exprimant le récepteur aux oestrogènes. En montrant l’importance de la SOD Mn et la DDB2 dans la croissance et l’invasion des cellules tumorales mammaires, l’ensemble de ce travail révèle ainsi ces deux protéines comme des marqueurs prédictifs potentiels de la progression tumorale, et ouvre de nombreuses perspectives en cancérologie mammaireRecently, our laboratory demonstrated for the first time, that Damaged DNA Binding 2 (DDB2) played a role as a negative transcriptional regulator on the mitochondrial superoxide dismutase (MnSOD) expression through its binding to a specific DNA sequence located into the promoter of MnSOD gene. DDB2 was known as a protein which participates in the nucleotide excision repair of DNA. The goal of this study was to define precisely the involvement of the both proteins in the growth of mammary adenocarcinoma cells, using experimental procedures to modulate their expression in the breast cancer cell lines. Our results show for the first time that MnSOD is overexpressed in the estrogen receptor (ER) negative and metastatic breast tumor cells, but not in normal epithelial mammary cells and ER-positive tumor cells. Inhibition of MnSOD expression stimulates proliferation but decreases the invasive ability and the metalloproteinase 9 activity of tumor cells. Elimination of H2O2 from the elevated MnSOD activity by addition of specific antioxidants decreases proliferation as well as invasive ability of tumor cells, suggesting that the role of MnSOD in the invasive ability of tumor cells is mediated by H2O2. We have shown too for the first time that DDB2 has an oncogenic activity in the ER-positive breast tumor cells, because its gene is overexpressed and stimulates the proliferation by activating the entry of cells in the G1/S transition phase and the S phase progression. In contrast to MnSOD, DDB2 expression is not observed in ER-negative breast tumor cells, but is higher in ER-positive than in ER-negative tumor samples from patients with breast carcinoma. Taken together, our findings demonstrate that both MnSOD and DDB2 play a role in the growth and invasiveness of tumor cells and may become a promising candidate as a predictive markers in breast cancer. More studies will be need to define molecular mechanism controlling this activity of these both proteins
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Minig, Vanessa. "Etude du mécanisme de régulation du gène et de l'importance biologique de la superoxyde dismutase à manganèse dans la croissance tumorale mammaire." Thesis, Nancy 1, 2009. http://www.theses.fr/2009NAN10032/document.
Повний текст джерелаАнотація:
La superoxyde dismutase à Manganèse (SOD Mn ou SOD2) est une enzyme importante dans la défense antioxydante, qui semble jouer un rôle mal défini dans le développement des tumeurs selon l’expression constitutive de son gène. Cependant, les mécanismes de régulation de cette expression constitutive sont mal connus, en particulier dans les cellules tumorales mammaires. Ce travail a reposé sur la mise en évidence préalable d’une protéine, appelée la Damaged DNA Binding 2 (DDB2) protein, se fixant spécifiquement sur la région promotrice du gène SOD2. La DDB2 est connue pour sa participation dans la réparation de l’ADN par excision de nucléotides. Dans un 1er temps, nous avons caractérisé la séquence d’ADN spécifiquement reconnue dans la région proximale du promoteur du gène SOD2, sur laquelle la DDB2 s’y fixe sous la forme d’un monomère, pour réguler négativement la transcription constitutive de la SOD Mn dans les cellules tumorales mammaires non métastatiques de type MCF-7. Par ailleurs, la DDB2 n’est pas impliquée dans le mécanisme d’induction du gène SOD2, lorsque les cellules MCF-7 sont exposées à des substances inductrices. En revanche, nous avons montré que l’absence de la protéine DDB2, associée à celle du facteur de transcription AP-2?, déjà connu comme répresseur du gène SOD2, entraîne une expression constitutive élevée de la SOD Mn dans les cellules tumorales mammaires métastatiques n’exprimant pas le récepteur aux œstrogènes (ER-). De plus, cette expression constitutive élevée est principalement dépendante du facteur de transcription Sp1. Dans un 2ème temps, nous avons évalué la signification biologique de la régulation de l’expression constitutive de la SOD Mn par la DDB2 dans les cellules tumorales mammaires. Nos résultats montrent que la DDB2 active la prolifération des cellules tumorales mammaires ER+, en exerçant sa régulation négative sur l’expression de la SOD Mn. Dans un 3ème temps, nous avons cherché à montrer les conséquences sur la croissance des cellules tumorales mammaires ER-, qui surexpriment naturellement la SOD Mn. Nos résultats révèlent que l’enzyme antioxydante joue un rôle important dans les mécanismes moléculaires impliqués dans le pouvoir invasif des cellules tumorales mammaires ER-. La surexpression de la SOD Mn, associée à un taux faible des enzymes éliminant l’H2O2, entraînent une augmentation du pouvoir invasif déjà élevé des cellules tumorales mammaires ER-, associée une augmentation de l’activité de la métalloprotéinase 9. L’élimination, en présence d’antioxydants, de l’H2O2 libéré par l’activité de la SOD Mn surexprimée, entraîne une inhibition à la fois de la croissance et des capacités invasives des cellules tumorales mammaires ER-. L’ensemble de ce travail contribue à mieux comprendre l’importance de la SOD Mn et du mécanisme de régulation de son gène dans la croissance et l’invasion tumorales. Ainsi ce travail révèle également la SOD Mn et la DDB2 comme de potentiels facteurs prédictifs de la progression tumorale mammaire. Enfin, la découverte de la nouvelle activité biologique de la DDB2 ouvre un vaste champ de perspectives intéressantes en cancérologie mammaireManganese superoxide dismutase (Mn SOD or SOD2) is an important enzyme in the antioxidizing defence, which seems to play an unclear role in the cancer development, according to the constitutive expression of its gene. However, the regulation of this constitutive expression is not totally known, particularly in the breast cancer cells. This work is based on a preliminary revealing that a protein, called Damaged DNA Binding 2 (DDB2), specifically binds the SOD2 gene promoter. The DDB2 is known for its involvement in the nucleotide excision repair. At first step, we characterized the specific DNA sequence recognized in the proximal area of the SOD2 gene promoter, on which a DDB2 monomer binds, in order to regulate negatively the Mn SOD transcription in the MCF-7 non metastatic breast cancer cells. Besides, DDB2 is not involved in the mechanism of SOD2 gene induction, when MCF-7 cells are exposed to induced substances. However, we showed that the lack of the DDB2 protein, associated with the lack of the AP-2a transcription factor, already known as a repressor of the SOD2 gene, lead to a high Mn SOD constitutive expression in the metastatic breast cancer cells. Furthermore, this high constitutive expression is mainly dependent of the Sp1 transcription factor. Secondly, we estimated the biological meaning of the regulation of the Mn SOD constitutive expression by the DDB2 in the breast cancer cells. Our results show that the DDB2 activates the positive ER breast cancer cell proliferation, by exercising its negative regulation on the Mn SOD expression. Thirdly, we tried to show the consequences on the negative ER breast cancer cell growth, which naturally and highly express the Mn SOD. Our results reveal that the antioxidizing enzyme plays an important role in the molecular mechanisms involved in the invasive capacities of the negative ER breast cancer cells. The high Mn SOD expression, associated in a decrease of the H2O2 detoxifying enzymes expression, enhance the negative ER breast cancer cell invasion and an increase of the matrix metallopeptidase-9 activity. The H2O2 elimination, with specific antioxidants, decreases both negative ER breast cancer cell growth and invasive capacities. This whole work contributes to better understand the Mn SOD importance and the mechanism of its gene regulation, in the tumoral growth and invasion. This work also reveals the Mn SOD and DDB2 as potential predictive factors of the breast cancer progress. Finally, the discovery of this new DDB2 biological activity opens a huge field of interesting perspectives in breast cancer research
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Domergue, Jérémy. "Modulation de l'activité SOD par contrôle de la sphère de coordination du Ni(II) dans des complexes bioinspirés." Thesis, Université Grenoble Alpes (ComUE), 2019. http://www.theses.fr/2019GREAV023.
Повний текст джерелаАнотація:
Le superoxyde O2●- est une espèce réactive de l’oxygène produite par de nombreux métabolismes chez les espèces vivant en condition aérobie. Ses propriétés radicalaires font de O2●- une espèce très réactive capable d’endommager les macromolécules présentes dans les cellules, conduisant entre autre au stress oxydant et à de possibles troubles neurodégénératifs. Pour se protéger, la Nature utilise des enzymes, appelées superoxydes dismutases (SOD), qui sont chargées de catalyser la dismutation du superoxyde en oxygène et peroxyde d’hydrogène. La dernière qui fut découverte est la NiSOD qui comporte un ion nickel dans son site actif. Contrairement aux autres types de SOD, celle-ci n’est pas présente chez l’homme et ne l’est que chez certaines bactéries comme Chlamydiae. Ainsi, cibler la NiSOD est une méthode prometteuse pour le développement de nouveaux antibiotiques. De même, le développement de nouveaux complexes biomimétiques des SOD peut conduire à de nouveaux agents thérapeutiques contre les maladies liées au stress oxydant. Notre projet consiste à développer de nouveaux modèles actifs de la NiSOD, avec comme stratégie l’utilisation de ligands peptidiques. Les deux principaux objectifs sont (1) de développer des catalyseurs de type SOD, actifs dans l’eau, mais aussi (2) d’acquérir des informations supplémentaires sur le mécanisme mis en jeu lors de la catalyse par la NiSOD, afin de mettre en évidence les intermédiaires clés et les différences majeures entre la NiSOD et les autres SODs présentes chez l’homme. Nos résultats montrent qu’une bonne activité catalytique peut être obtenue même avec une sphère de coordination différente de celle de l’enzyme, et mettent en évidence des facteurs clés pour l’activité. De plus, des études mécanistiques tendent à montrer un mécanisme en sphère interne pour la réduction du superoxydeThe superoxide radical anion, O2●-, is generated by many life processes. Its radical properties make it a highly reactive species able to damage all macromolecules contributing to the pathogenesis of many diseases including neurodegenerative disorders. In order to protect cells against O2●-, Nature uses superoxide dismutases (SODs) which catalyze the dismutation of O2●- into hydrogen peroxide and oxygen. The last discovered SOD contains a nickel cofactor. Importantly the NiSOD is found in several pathogenic bacteria but not in humans. Therefore targeting the NiSOD is a promising approach to develop antibiotics. Secondly, the development of novel SOD mimics may have potential uses as therapeutic agents in oxidative stress-related diseases. Our project aims at developing innovative active NiSOD mimics, based on the use of peptide-based ligands with two main objectives: (i) to develop efficient SOD like catalysts, active in water, displaying antioxidant properties for potential therapeutic applications and (ii) to contribute to the full understanding of the catalytic mechanism of the NiSOD to highlight the specific key elements that differentiate NiSOD from the human MnSOD for the design of potential antibiotics. Our results show that, even with a coordination sphere different from the one in the enzyme, a good catalytic activity can be obtained. Key elements for the activity are also determined. Moreover, mechanistic studies indicates an inner sphere mechanism for superoxide reduction
Частини книг з теми "Mime de Superoxyde Dismutase (SOD)"
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Shimizu, Takahiko, Hidetoshi Nojiri, and Takuji Shirasawa. "Tissue-Specific Deletion of Manganese Superoxide Dismutase (Mn-SOD) in Mice." In Systems Biology of Free Radicals and Antioxidants, 475–87. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-30018-9_21.
Повний текст джерела
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"The Role of Superoxide Dismutase in Age-Related and Noise-Induced Hearing Loss: Clues from SOD1 Knockout Mice." In Handbook of Mouse Auditory Research, 503–18. CRC Press, 2001. http://dx.doi.org/10.1201/9781420038736-40.
Повний текст джерелаТези доповідей конференцій з теми "Mime de Superoxyde Dismutase (SOD)"
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Zelko, Igor N., Marcus W. Stepp, and Rodney J. Folz. "Live In-Vivo Imaging Of Extracellular Superoxide Dismutase (EC-SOD) Promoter Activity In Transgenic Mice." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1275.
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Tanaka, Ken-ichiro, and Tohru Mizushima. "Therapeutic Effect Of Lecithinized Superoxide Dismutase (PC-SOD) On Elastase-induced Pulmonary Emphysema In Mice." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4424.
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Longoria, C., J. Ibrahim, J. Liao, N. Cheong, E. N. Grayck, and R. C. Savani. "Extracellular Superoxide Dismutase (EC-SOD) Knockout Mice Have Worse Alveolarization, Inflammation and Cytokine Elaboration After Neonatal Hyperoxia Exposure." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5312.
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Mizushima, Tohru, Ken-ichiro Tanaka, and Arata Azuma. "Therapeutic Effect Of Lecithinized Superoxide Dismutase (PC-SOD) On Idiopathic Pulmonary Fibrosis In Humans And Bleomycin-induced Pulmonary Fibrosis In Mice." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1052.
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