Relevant bibliographies by topics / MnSOD mimic

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Academic literature on the topic 'MnSOD mimic'

Author: Grafiati
Published: 23 September 2022
Last updated: 28 September 2022

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Journal articles on the topic "MnSOD mimic"

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ROGERS, Richard J., Sarah E. CHESROWN, Shiuhyang KUO, Joan M. MONNIER, and Harry S. NICK. "Cytokine-inducible enhancer with promoter activity in both the rat and human manganese-superoxide dismutase genes." Biochemical Journal 347, no. 1 (March 27, 2000): 233–42. http://dx.doi.org/10.1042/bj3470233.

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Diverse pro-inflammatory mediators regulate transcription of the gene (MnSOD) encoding the mitochondrial anti-oxidant protein manganese-superoxide dismutase. Understanding the regulation of this gene is crucial to comprehending its role in cytoprotection. In transfected lung epithelial cells, a human-growth-hormone reporter gene system was utilized to identify a potential enhancer in the MnSOD genomic fragment previously shown to contain multiple DNase-I-hypersensitive sites. Northern analysis demonstrated a 10-20-fold increase in response to pro-inflammatory mediators. Inclusion of the MnSOD genomic fragment in reporter constructs was necessary to mimic these stimulus-dependent endogenous levels. The inducible enhancer element was localized to a 260 bp fragment in intron 2, coinciding with a previously defined DNase-I-hypersensitive site. This element functions in an orientation- and position-independent manner as well as with the heterologous thymidine kinase promoter. In addition, we have demonstrated that a homologous sequence within the human MnSOD gene exhibits identical enhancer activity. A novel characteristic of the rat and human enhancer elements involves the ability to promote cytokine-inducible transcription in the absence of a classical promoter.
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Yuan, Yanggang, Hui Wang, Yingyi Wu, Bo Zhang, Ningning Wang, Huijuan Mao, and Changying Xing. "P53 Contributes to Cisplatin Induced Renal Oxidative Damage via Regulating P66shc and MnSOD." Cellular Physiology and Biochemistry 37, no. 4 (2015): 1240–56. http://dx.doi.org/10.1159/000430247.

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Background/Aims: Cisplatin is widely used to treat malignancies. However, its major limitation is the development of dose-dependent nephrotoxicity. The precise mechanisms of cisplatin-induced kidney damage remain unclear. Previous study demonstrated the central role of mitochondrial ROS (mtROS) in the pathogenesis of cisplatin nephrotoxicity. The purpose of this study was to explore the mechanism of mtROS regulation in cisplatin nephrotoxicity. Methods: p53, MnSOD and p66shc were detected at mRNA and protein levels by qPCR and western blot in HK2 cells. mtROS levels were determined by DCFDA and MitoSOX staining. Cell viability and cell apoptosis were accessed by CCK-8 assay, TUNEL assay and flow cytometry, respectivesly. siRNAs were used to knock down p53 and p66shc expression and subsequent changes were observed. In vivo assays using a mouse model of cisplatin-induced acute kidney injury were used to validate the in vitro results. Results: In HK2 cells, cisplatin exposure decreased the MnSOD and increased the expression of p53 and p66shc. MnTBAP, a MnSOD mimic, blocked cisplatin-induced the generation of mtROS and cell injury. P66shc and p53 siRNAs rendered renal cells resistant to cisplatin-induced mtROS production and cell death. Furthermore, knockdown of p53 restored MnSOD and inhibiting p66shc. Consistent with these results, we revealed that p53 inhibitor reduced cisplatin-induced oxidative stress and apoptosis by regulating MnSOD and p66shc in the kidney of cisplatin-treated mice. Conclusion: Our study identifies activation of p53 signalling as a potential strategy for reducing the nephrotoxicity associated with cisplatin treatments and, as a result, broadens the therapeutic window of this chemotherapeutic agent.
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Dewhirst, M. W., K. Ashcraft, I. Batinic-Haberle, I. Spasojevic, and D. M. Brizel. "A Novel Mnsod Mimic Widens the Therapeutic Margin by Simultaneously Radioprotecting Normal Tissue and Radiosensitizing Tumor." International Journal of Radiation Oncology*Biology*Physics 88, no. 2 (February 2014): 468. http://dx.doi.org/10.1016/j.ijrobp.2013.11.028.

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Mathieu, Emilie, Anne-Sophie Bernard, Nicolas Delsuc, Elodie Quévrain, Géraldine Gazzah, Barry Lai, Florian Chain, et al. "A Cell-Penetrant Manganese Superoxide Dismutase (MnSOD) Mimic Is Able To Complement MnSOD and Exerts an Antiinflammatory Effect on Cellular and Animal Models of Inflammatory Bowel Diseases." Inorganic Chemistry 56, no. 5 (February 15, 2017): 2545–55. http://dx.doi.org/10.1021/acs.inorgchem.6b02695.

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Inclán, Mario, María Teresa Albelda, Salvador Blasco, Carolina Serena, Javier Ugarte Chicote, Antonio García-España, and Enrique García-España. "Mn(II) Complexes of Enlarged Scorpiand-Type Azamacrocycles as Mimetics of MnSOD Enzyme." Applied Sciences 12, no. 5 (February 26, 2022): 2447. http://dx.doi.org/10.3390/app12052447.

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Living organisms depend on superoxide dismutase (SOD) enzymes to shield themselves from the deleterious effects of superoxide radical. In humans, alterations of these protective mechanisms have been linked to the pathogenesis of many diseases. However, the therapeutic use of the native enzyme is hindered by, among other things, its high molecular size, low stability, and immunogenicity. For this reason, synthetic SOD mimetic compounds of low molecular weight may have therapeutic potential. We present here three low-molecular-weight compounds, whose Mn2+ complexes can mimic, at least partially, the protective activity of SOD-enzymes. These compounds were characterized by NMR, potentiometry, and, to test whether they have protective activity in vitro, by their capacity to restore the growth of SOD-deficient strains of E. coli. In this report, we provide evidence that these compounds form stable complexes with Mn2+ and have an in vitro protective effect, restoring up to 75% the growth of the SOD-deficient E. coli.
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Pedullà, Marcella, Riccardo d'Aquino, Vincenzo Desiderio, Francesco de Francesco, Andrew Puca, and Gianpaolo Papaccio. "MnSOD mimic compounds can counteract mechanical stress and islet β cell apoptosis, although at appropriate concentration ranges." Journal of Cellular Physiology 212, no. 2 (February 20, 2007): 432–38. http://dx.doi.org/10.1002/jcp.21034.

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7

González Arbeláez, Luisa F., Ignacio A. Pérez Núñez, and Susana M. Mosca. "Gsk-3βInhibitors Mimic the Cardioprotection Mediated by Ischemic Pre- and Postconditioning in Hypertensive Rats." BioMed Research International 2013 (2013): 1–11. http://dx.doi.org/10.1155/2013/317456.

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The aim of this study was to examine the effects of GSK-3βinhibitors compared with PRE and POS in spontaneously hypertensive rats (SHR). Isolated hearts were submitted to the following protocols: IC: 45 min global ischemia (GI) and 1-hour reperfusion (R); PRE: a cycle of 5 min GI and 10 minutes of R prior to 45 min GI; POS: three cycles of 30 sec GI/30 sec R at the start of R. Other hearts received lithium chloride (LiCl) or indirubin-3′-monoxime,5-iodo-(IMI) as GSK-3βinhibitors. All interventions reduced the infarct size observed in IC group. The expressions of P-GSK-3βand P-Akt decreased in IC and were restored after PRE, POS, and GSK-3βinhibitors treatments. An increase of cytosolic MnSOD activity and lipid peroxidation and a decrease of GSH content observed in IC hearts were attenuated in PRE, POS, and LiCl or IMI treatments. An increase of P-GSK-3β/VDAC physical association and a partial recovery of mitochondrial permeability were also detected after interventions. These data show that, in SHR hearts, GSK-3βinhibitors mimic the cardioprotection afforded by PRE and POS and suggest that a decrease in mitochondrial permeability mediated by P-GSK-3β/VDAC interaction is a crucial event.
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Karlsson, Jan Olof G., Per Jynge, and Louis J. Ignarro. "May Mangafodipir or Other SOD Mimetics Contribute to Better Care in COVID-19 Patients?" Antioxidants 9, no. 10 (October 10, 2020): 971. http://dx.doi.org/10.3390/antiox9100971.

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is characterized by massive inflammation of the arterial endothelium accompanied by vasoconstriction and widespread pulmonary micro thrombi. As a result, due to the destruction of nitric oxide (•NO) by inflammatory superoxide (O2•−), pulmonary •NO concentration ceases, resulting in uncontrolled platelet aggregation and massive thrombosis, which kills the patients. Introducing •NO by inhalation (INO) may replace the loss of endothelium-derived •NO. The first results from clinical trials with INO in SARS-CoV-2 patients show a rapid and sustained improvement in cardiopulmonary function and decreased inflammation. An ongoing phase III study is expected to confirm the method’s efficacy. INO may hence become a first line treatment in SARS-CoV-2 patients. However, due to the rapid inactivation of •NO by deoxyhemoglobin to nitrate, pulmonary administration of •NO will not protect remote organs. Another INO-related pharmacological approach to protect SARS-CoV-2 patients from developing life-threatening disease is to inhibit the O2•−-driven destruction of •NO by neutralizing inflammatory O2•−. By making use of low molecular weight compounds that mimic the action of the enzyme manganese superoxide dismutase (MnSOD). The MnSOD mimetics of the so-called porphyrin type (e.g., AEOL 10150), salen type (e.g., EUK-8) and cyclic polyamine type (e.g., M40419, today known as GC4419 and avasopasem manganese) have all been shown to positively affect the inflammatory response in lung epithelial cells in preclinical models of chronic obstructive pulmonary disease. The Manganese diPyridoxyL EthylDiamine (MnPLED)-type mangafodipir (manganese dipyridoxyl diphosphate—MnDPDP), a magnetic resonance imaging (MRI) contrast agent that possesses MnSOD mimetic activity, has shown promising results in various forms of inflammation, in preclinical as well as clinical settings. Intravenously administration of mangafodipir will, in contrast to INO, reach remote organs and may hence become an important supplement to INO. From the authors’ viewpoint, it appears logical to test mangafodipr in COVID-19 patients at risk of developing life-threatening SARS-CoV-2. Five days after submission of the current manuscript, Galera Pharmaceuticals Inc. announced the dosing of the first patient in a randomized, double-blind pilot phase II clinical trial with GC4419 for COVID-19. The study was first posted on ClinicalTrials.gov (Identifier: NCT04555096) 18 September 2020.
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Lowes, Damon A., and Helen F. Galley. "Mitochondrial protection by the thioredoxin-2 and glutathione systems in an in vitro endothelial model of sepsis." Biochemical Journal 436, no. 1 (April 27, 2011): 123–32. http://dx.doi.org/10.1042/bj20102135.

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Oxidative stress and mitochondrial dysfunction are common features in patients with sepsis and organ failure. Within mitochondria, superoxide is converted into hydrogen peroxide by MnSOD (manganese-containing superoxide dismutase), which is then detoxified by either the mGSH (mitochondrial glutathione) system, using the enzymes mGPx-1 (mitochondrial glutathione peroxidase-1), GRD (glutathione reductase) and mGSH, or the TRX-2 (thioredoxin-2) system, which uses the enzymes PRX-3 (peroxiredoxin-3) and TRX-2R (thioredoxin reductase-2) and TRX-2. In the present paper we investigated the relative contribution of these two systems, using selective inhibitors, in relation to mitochondrial dysfunction in endothelial cells cultured with LPS (lipopolysaccharide) and PepG (peptidoglycan). Specific inhibition of both the TRX-2 and mGSH systems increased the intracellular total radical production (P<0.05) and reduced mitochondrial membrane potentials (P<0.05). Inhibition of the TRX-2 system, but not mGSH, resulted in lower ATP production (P<0.001) with high metabolic activity (P<0.001), low oxygen consumption (P<0.001) and increased lactate production (P<0.001) and caspase 3/7 activation (P<0.05). Collectively these results show that the TRX-2 system appears to have a more important role in preventing mitochondrial dysfunction than the mGSH system in endothelial cells under conditions that mimic a septic insult.
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10

Wing, Lih-Yuh Chen, Ya-Chi Chen, Yu-Yin Shih, Jung-Chien Cheng, Yiu-Jiuan Lin, and Meei Jyh Jiang. "Effects of Oral Estrogen on Aortic ROS-Generating and -Scavenging Enzymes and Atherosclerosis in apoE-Deficient Mice." Experimental Biology and Medicine 234, no. 9 (September 2009): 1037–46. http://dx.doi.org/10.3181/0811-rm-332.

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The effect of hormone replacement therapy (HRT) on cardiovascular diseases remains controversial. Studies conducted on postmenopausal women indicate that oral HRT increases risk factors that may counteract the atheroprotective effect of estrogen. However, the effects of estrogen on atherosclerosis have been examined using subcutaneous estrogen in most animal studies, which points to the need for evaluating the effect of oral estrogen. Reactive oxygen species (ROS) have emerged as critical factors in the pathogenesis of atherosclerosis. This study examined the effect of long-term oral estrogen treatment on aortic oxidative stress and atherosclerosis in female apoE−/− mice to mimic HRT in humans. Ovariectomized apoE−/− mice were given 6 μg/day of oral 17β-estradiol (E2) or control vehicle for 12 weeks. Estrogen treatment reduced atherosclerotic lesions by 38% (E2: 0.20 ± 0.01 mm2/section; control vehicle: 0.32 ± 0.02 mm2/section) and intima by 32% (E2: 0.44 ± 0.02 mm2/section; control vehicle: 0.65 ± 0.04 mm2/section) in the aortic root. Serum levels of total and low-density lipoprotein cholesterol were significantly decreased after estrogen treatment. Aortic superoxide anion levels and the expression of NAD(P)H oxidase subunit p22phox markedly decreased, and two ROS scavenging enzymes, Cu/ZnSOD and MnSOD, were upregulated after estrogen treatment. Estrogen at physiological concentration inhibited tumor necrosis factor-α-stimulated NAD(P)H oxidase activity in both cultured smooth muscle cells and peritoneal macrophages. These results showed that long-term oral estrogen treatment reduces ROS levels and atherosclerosis progression in apoE−/− mice. Oral estrogen alters ROS-generating and -scavenging enzyme expression, suggesting that anti-oxidative actions in the vessel wall contribute to atheroprotective effects of estrogen.
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Dissertations / Theses on the topic "MnSOD mimic"

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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.

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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 MICI
The 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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