scholarly journals The Role of Manganese Superoxide Dismutase in Skin Cancer

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Delira Robbins ◽  
Yunfeng Zhao
Keyword(s):  
Manganese Superoxide Dismutase ◽  
Skin Diseases ◽  
Mouse Skin ◽  
Oxidative Injury ◽  
Antioxidant Response ◽  
Protective Effects ◽  
Disease States ◽  
Novel Approach ◽  
Manganese Superoxide ◽  
Expression And Activity

Recent studies have shown that antioxidant enzyme expression and activity are drastically reduced in most human skin diseases, leading to propagation of oxidative stress and continuous disease progression. However, antioxidants, an endogenous defense system against reactive oxygen species (ROS), can be induced by exogenous sources, resulting in protective effects against associated oxidative injury. Many studies have shown that the induction of antioxidants is an effective strategy to combat various disease states. In one approach, a SOD mimetic was applied topically to mouse skin in the two-stage skin carcinogenesis model. This method effectively reduced oxidative injury and proliferation without interfering with apoptosis. In another approach, Protandim, a combination of 5 well-studied medicinal plants, was given via dietary administration and significantly decreased tumor incidence and multiplicity by 33% and 57%, respectively. These studies suggest that alterations in antioxidant response may be a novel approach to chemoprevention. This paper focuses on how regulation of antioxidant expression and activity can be modulated in skin disease and the potential clinical implications of antioxidant-based therapies.

scholarly journals Neutral Sphingomyelinase Modulation in the Protective/Preventive Role of rMnSOD from Radiation-Induced Damage in the Brain

2019 ◽  
Vol 20 (21) ◽  
pp. 5431 ◽  
Author(s):  
Samuela Cataldi ◽  
Antonella Borrelli ◽  
Maria Rachele Ceccarini ◽  
Irina Nakashidze ◽  
Michela Codini ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Manganese Superoxide Dismutase ◽  
Nuclear Research ◽  
Protective Effects ◽  
Manganese Superoxide ◽  
Additional Group ◽  
Gene And Protein Expression ◽  
Radiation Induced ◽  
The Brain ◽  
Preventive Role

Studies on the relationship between reactive oxygen species (ROS)/manganese superoxide dismutase (MnSOD) and sphingomyelinase (SMase) are controversial. It has been demonstrated that SMase increases the intracellular ROS level and induces gene expression for MnSOD protein. On the other hand, some authors showed that ROS modulate the activation of SMase. The human recombinant manganese superoxide dismutase (rMnSOD) exerting a radioprotective effect on normal cells, qualifies as a possible pharmaceutical tool to prevent and/or cure damages derived from accidental exposure to ionizing radiation. This study aimed to identify neutral SMase (nSMase) as novel molecule connecting rMnSOD to its radiation protective effects. We used a new, and to this date, unique, experimental model to assess the effect of both radiation and rMnSOD in the brain of mice, within a collaborative project among Italian research groups and the Joint Institute for Nuclear Research, Dubna (Russia). Mice were exposed to a set of minor γ radiation and neutrons and a spectrum of neutrons, simulating the radiation levels to which cosmonauts will be exposed during deep-space, long-term missions. Groups of mice were treated or not-treated (controls) with daily subcutaneous injections of rMnSOD during a period of 10 days. An additional group of mice was also pretreated with rMnSOD for three days before irradiation, as a model for preventive measures. We demonstrate that rMnSOD significantly protects the midbrain cells from radiation-induced damage, inducing a strong upregulation of nSMase gene and protein expression. Pretreatment with rMnSOD before irradiation protects the brain with a value of very high nSMase activity, indicating that high levels of activity might be sufficient to exert the rMnSOD preventive role. In conclusion, the protective effect of rMnSOD from radiation-induced brain damage may require nSMase enzyme.

scholarly journals Cardiac Electrophysiological Alterations in Heart/Muscle-Specific Manganese-Superoxide Dismutase-Deficient Mice: Prevention by a Dietary Antioxidant Polyphenol

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Tadahiro Sunagawa ◽  
Takahiko Shimizu ◽  
Akio Matsumoto ◽  
Motoyuki Tagashira ◽  
Tomomasa Kanda ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Action Potential ◽  
Heart Muscle ◽  
Chronic Exposure ◽  
Manganese Superoxide Dismutase ◽  
Left Ventricular ◽  
Protective Effects ◽  
Manganese Superoxide ◽  
Dietary Antioxidant

Cardiac electrophysiological alterations induced by chronic exposure to reactive oxygen species and protective effects of dietary antioxidant have not been thoroughly examined. We recorded surface electrocardiograms (ECG) and evaluated cellular electrophysiological abnormalities in enzymatically-dissociated left ventricular (LV) myocytes in heart/muscle-specific manganese-superoxide dismutase-deficient (H/M-Sod2−/−) mice, which exhibit dilated cardiomyopathy due to increased oxidative stress. We also investigated the influences of intake of apple polyphenols (AP) containing mainly procyanidins with potent antioxidant activity. The QRS and QT intervals of ECG recorded in H/M-Sod2−/−mice were prolonged. The effective refractory period in the LV myocardium of H/M-Sod2−/−mice was prolonged, and susceptibility to ventricular tachycardia or fibrillation induced by rapid ventricular pacing was increased. Action potential duration in H/M-Sod2−/−LV myocytes was prolonged, and automaticity was enhanced. The density of the inwardly rectifier K+current (IK1) was decreased in the LV cells of H/M-Sod2−/−mice. The AP intake partially improved these electrophysiological alterations and extended the lifespan in H/M-Sod2−/−mice. Thus, chronic exposure of the heart to oxidative stress produces a variety of electrophysiological abnormalities, increased susceptibility to ventricular arrhythmias, and action potential changes associated with the reduced density ofIK1. Dietary intake of antioxidant nutrients may prevent oxidative stress-induced electrophysiological disturbances.

scholarly journals Manganese Superoxide Dismutase-Mediated Inside-Out Signaling in HaCaT Human Keratinocytes and SKH-1 Mouse Skin

2014 ◽  
Vol 20 (15) ◽  
pp. 2347-2360 ◽  
Author(s):  
Aaron K. Holley ◽  
Yong Xu ◽  
Teresa Noel ◽  
Vasudevan Bakthavatchalu ◽  
Ines Batinic-Haberle ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Manganese Superoxide Dismutase ◽  
Mouse Skin ◽  
Human Keratinocytes ◽  
Manganese Superoxide ◽  
Inside Out

scholarly journals A Gel Formulation Containing a New Recombinant Form of Manganese Superoxide Dismutase: A Clinical Experience Based on Compassionate Use-Safety of a Case Report

2016 ◽  
Vol 2016 ◽  
pp. 1-4
Author(s):  
Lucia Grumetto ◽  
Antonio Del Prete ◽  
Giovanni Ortosecco ◽  
Antonella Borrelli ◽  
Salvatore Del Prete ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Case Report ◽  
Manganese Superoxide Dismutase ◽  
Recombinant Form ◽  
Term Therapy ◽  
Protective Effects ◽  
Manganese Superoxide ◽  
Gel Preparation ◽  
The Right ◽  
Long Term Therapy

Background. We report a case of bilateral posterior subcapsular cataracts (PSCs) in a 24-year-old man with an allergic conjunctivitis history caused by a long-term therapy with glucocorticoids.Case Presentation. The patient showed a visual acuity of 9/10 for both eyes. He followed a therapy with ketotifen and bilastine for four years. During the last six months before our evaluation, he was treated with chloramphenicol and betamethasone, interrupted for onset of cataracts and increased intraocular pressure. We treated him with ophthalmic gel preparation containing a new recombinant form of manganese superoxide dismutase (rMnSOD) at a concentration of 12.5 μg/mL, only for the right eye, while left eye was treated with standard protocol of Bendazac-lysine g 0.5.Conclusion. This case report shows the protective effects of rMnSOD versus PSC disease, probably due to the capacity of rMnSOD of countering free radical species.

Bilobalide protects astrocytes from oxygen and glucose deprivation‐induced oxidative injury by upregulating manganese superoxide dismutase

2019 ◽  
Vol 33 (9) ◽  
pp. 2329-2336 ◽  
Author(s):  
Jun Xiang ◽  
Jingsi Zhang ◽  
Xiaofang Cai ◽  
Feng Yang ◽  
Wen Zhu ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Manganese Superoxide Dismutase ◽  
Oxidative Injury ◽  
Glucose Deprivation ◽  
Oxygen And Glucose Deprivation ◽  
Manganese Superoxide

scholarly journals Enhanced Peroxynitrite Formation Is Associated with Vascular Aging

2000 ◽  
Vol 192 (12) ◽  
pp. 1731-1744 ◽  
Author(s):  
Bernd van der Loo ◽  
Ralf Labugger ◽  
Jeremy N. Skepper ◽  
Markus Bachschmid ◽  
Juliane Kilo ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Superoxide Dismutase ◽  
Aging Process ◽  
Manganese Superoxide Dismutase ◽  
No Synthase ◽  
Vascular Aging ◽  
Enos Expression ◽  
Manganese Superoxide ◽  
O2 Production ◽  
Expression And Activity

Vascular aging is mainly characterized by endothelial dysfunction. We found decreased free nitric oxide (NO) levels in aged rat aortas, in conjunction with a sevenfold higher expression and activity of endothelial NO synthase (eNOS). This is shown to be a consequence of age-associated enhanced superoxide (·O2−) production with concomitant quenching of NO by the formation of peroxynitrite leading to nitrotyrosilation of mitochondrial manganese superoxide dismutase (MnSOD), a molecular footprint of increased peroxynitrite levels, which also increased with age. Thus, vascular aging appears to be initiated by augmented ·O2− release, trapping of vasorelaxant NO, and subsequent peroxynitrite formation, followed by the nitration and inhibition of MnSOD. Increased eNOS expression and activity is a compensatory, but eventually futile, mechanism to counter regulate the loss of NO. The ultrastructural distribution of 3-nitrotyrosyl suggests that mitochondrial dysfunction plays a major role in the vascular aging process.

scholarly journals Interplay between Intravitreal RvD1 and Local Endogenous Sirtuin-1 in the Protection from Endotoxin-Induced Uveitis in Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
S. Rossi ◽  
C. Di Filippo ◽  
C. Gesualdo ◽  
F. Testa ◽  
M. C. Trotta ◽  
...  
Keyword(s):  
Manganese Superoxide Dismutase ◽  
Specific Inhibitor ◽  
Sirtuin 1 ◽  
Formyl Peptide Receptor ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Resolvin D1 ◽  
Manganese Superoxide ◽  
Sprague Dawley Rats ◽  
Formyl Peptide

Rat endotoxin-induced uveitis (EIU) is a well-established model of human uveitis. In this model, intravitreal injection of resolvin D1 (RvD1, 10–100–1000 ng/kg) 1 hour after subcutaneous treatment of Sprague-Dawley rats with lipopolysaccharide (LPS, 200 μg/rat) significantly prevented the development of uveitis into the eye. RvD1 dose-dependently increased the expression of sirtuin-1 (SIRT1) within the eye, while it decreased the expression of acetyl-p53 and acetyl-FOXO1. These effects were accompanied by local downregulation of some microRNAs related to the expression and activity of SIRT1. These were miR-195-5p, miR-200a-3p, miR-34a-5p, and miR-145-5p. An increase of manganese superoxide dismutase and decrease of caspase 3 were evident after RvD1 treatment. In another set of experiments, the protective effects of RvD1 (1000 ng/kg) were partly abolished by the pretreatment of the rats with EX527 (10 mg/kg/day, i.p.), a specific inhibitor of SIRT1 activity, for 7 days prior to the induction of EIU in rats. Similarly, the effects of RvD1 (1000 ng/kg) on the SIRT1 protein expression were abolished by Boc2,N-t-butoxycarbonyl-PLPLP, a specific formyl-peptide receptor type 2/lipoxin A receptor antagonist. Therefore, an interplay of the SIRT1 activity on the RvD1 mediated resolution of EIU is argued.

scholarly journals Decreases in manganese superoxide dismutase expression and activity contribute to oxidative stress in persistent pulmonary hypertension of the newborn

2012 ◽  
Vol 303 (10) ◽  
pp. L870-L879 ◽  
Author(s):  
Adeleye J. Afolayan ◽  
Annie Eis ◽  
Ru-Jeng Teng ◽  
Ivane Bakhutashvili ◽  
Sushma Kaul ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Superoxide Dismutase ◽  
Manganese Superoxide Dismutase ◽  
Pulmonary Arteries ◽  
Tyrosine Nitration ◽  
Enos Expression ◽  
Manganese Superoxide ◽  
Expression And Activity

A rapid increase in the synthesis and release of nitric oxide (NO) facilitates the pulmonary vasodilation that occurs during birth-related transition. Alteration of this transition in persistent pulmonary hypertension of the newborn (PPHN) is associated with impaired function of endothelial nitric oxide synthase (eNOS) and an increase in oxidative stress. We investigated the hypothesis that a decrease in expression and activity of mitochondrial localized manganese superoxide dismutase (MnSOD) in pulmonary artery endothelial cells (PAEC) increases oxidative stress and impairs eNOS function in PPHN. We isolated PAEC and pulmonary arteries from fetal lambs with PPHN induced by prenatal ductus arteriosus ligation or sham ligation (control). We investigated MnSOD expression and activity, tyrosine nitration of MnSOD, and mitochondrial O2− levels in PAEC from control and PPHN lambs. We introduced exogenous MnSOD via an adenoviral vector (ad-MnSOD) transduction into PAEC and pulmonary arteries of PPHN lambs. The effect of ad-MnSOD was investigated on: mitochondrial O2− levels, MnSOD and eNOS expression and activity, intracellular hydrogen peroxide (H2O2) levels, and catalase expression in PAEC. MnSOD mRNA and protein levels and activity were decreased and MnSOD tyrosine nitration was increased in PPHN-PAEC. ad-MnSOD transduction of PPHN-PAEC increased its activity two- to threefold, decreased mitochondrial O2− levels, and increased H2O2 levels and catalase expression. ad-MnSOD transduction improved eNOS expression and function and the relaxation response of PPHN pulmonary arteries. Our observations suggest that decreased MnSOD expression and activity contribute to the endothelial dysfunction observed in PPHN.

Heterozygous Deficiency of Manganese Superoxide Dismutase in Mice (Mn-SOD+/-): A Novel Approach to Assess the Role of Oxidative Stress for the Development of Nitrate Tolerance

2005 ◽  
Vol 68 (3) ◽  
pp. 579-588 ◽  
Author(s):  
Andreas Daiber ◽  
Matthias Oelze ◽  
Silke Sulyok ◽  
Meike Coldewey ◽  
Eberhard Schulz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Manganese Superoxide Dismutase ◽  
Nitrate Tolerance ◽  
Novel Approach ◽  
Manganese Superoxide ◽  
Heterozygous Deficiency
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