Pertussis toxin alters the concentration and turnover of manganese superoxide dismutase in rat lung

1996 ◽  
Vol 271 (6) ◽  
pp. L875-L879
Author(s):  
A. Berkovich ◽  
D. Massaro ◽  
L. B. Clerch
Keyword(s):  
Superoxide Dismutase ◽  
Pertussis Toxin ◽  
Manganese Superoxide Dismutase ◽  
Specific Activity ◽  
Oxygen Toxicity ◽  
Translational Efficiency ◽  
Sod Activity ◽  
Manganese Superoxide ◽  
Guanine Nucleotide Binding ◽  
Nucleotide Binding Proteins

Treatment of rats with pertussis toxin (PTX) decreases the activity of manganese superoxide dismutase (Mn-SOD) in the lung and results in oxygen toxicity in air (L. B. Clerch, G. Neithardt, U. Spencer, J. A. Melendez, G. D. Massaro, and D. Massaro. J. Clin. Invest. 93: 2482-2489, 1994). To examine aspects of the mechanism of the PTX-induced fall in Mn-SOD activity, we injected rats with PTX (50 micrograms/kg), killed the rats 72 h later, and measured the activity, concentration, specific activity, and turnover of Mn-SOD in the lung. Treatment with PTX caused an approximately 50% fall in Mn-SOD activity and Mn-SOD concentration but no change in Mn-SOD specific activity. PTX also caused an increase in Mn-SOD mRNA concentration, a fall in Mn-SOD synthesis, and an increase in the half-life of Mn-SOD and general proteins. We conclude the PTX-induced low concentration of Mn-SOD is due to a decrease of translational efficiency. We suggest that, under normoxic conditions, signal transduction via heterotrimeric guanine nucleotide binding proteins regulates the expression of Mn-SOD at the level of translation and Mn-SOD degradation.

Alpha 1-adrenergic stimulation induces cardiac tolerance to hypoxia via induction and activation of Mn-SOD

1996 ◽  
Vol 271 (4) ◽  
pp. H1356-H1362 ◽  
Author(s):  
N. Yamashita ◽  
M. Nishida ◽  
S. Hoshida ◽  
J. Igarashi ◽  
M. Hori ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Creatine Kinase ◽  
Cardiac Myocytes ◽  
Total Protein ◽  
Manganese Superoxide Dismutase ◽  
Specific Activity ◽  
Adrenergic Stimulation ◽  
Sod Activity ◽  
Manganese Superoxide ◽  
Tolerance To Hypoxia

We examined whether or not alpha 1-adrenergic stimulation increases the tolerance of the heart to ischemia using a hypoxia-reoxygenation model of cardiac myocytes. After exposure to norepinephrine (NE; 0.2 microM) for 24 h, the manganese superoxide dismutase (Mn-SOD) content and activity in the cells were increased from 0.61 +/- 0.03 to 0.87 +/- 0.04 microgram/dish and 22 +/- 1 to 55 +/- 4 U/dish, respectively. The specific activity of Mn-SOD was also increased from 36 to 63 U/microgram Mn-SOD protein after the stimulation with NE. Prazosin (2 microM) abolished the increase in Mn-SOD activity (U/mg total protein). Creatine kinase (CK) release after hypoxia (PO2 7 mmHg; 3 h)-reoxygenation (1 h) from cells pretreated with NE in the presence of propranolol and yohimbine for 24 h was attenuated by 48% compared with that from cells without NE stimulation. When antisense oligodeoxyribonucleotides to Mn-SOD were added to myocyte cultures, the increase in Mn-SOD activity (U/mg total protein) and the attenuation of CK release after the addition of NE in the presence of propranolol and yohimbine were not observed. These results suggest that alpha 1-adrenergic stimulation increases the tolerance of myocytes to hypoxia through induction and activation of Mn-SOD.

Regulation of lung manganese superoxide dismutase: species variation in response to lipopolysaccharide

1999 ◽  
Vol 276 (5) ◽  
pp. L705-L708 ◽  
Author(s):  
Ghenima Dirami ◽  
Donald Massaro ◽  
Linda Biadasz Clerch
Keyword(s):  
Superoxide Dismutase ◽  
Manganese Superoxide Dismutase ◽  
Critical Role ◽  
Mouse Lung ◽  
Translational Efficiency ◽  
Species Variation ◽  
Sod Activity ◽  
Mrna Concentration ◽  
Manganese Superoxide ◽  
Lps Treatment

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.

Rat lung antioxidant enzymes: differences in perinatal gene expression and regulation

1992 ◽  
Vol 263 (4) ◽  
pp. L466-L470 ◽  
Author(s):  
L. B. Clerch ◽  
D. Massaro
Keyword(s):  
Gene Expression ◽  
Superoxide Dismutase ◽  
Antioxidant Enzymes ◽  
Manganese Superoxide Dismutase ◽  
Late Gestation ◽  
Postnatal Exposure ◽  
Sod Activity ◽  
Copper Zinc Superoxide Dismutase ◽  
Manganese Superoxide ◽  
Copper Zinc

The lung activity of the antioxidant enzymes (AOEs) copper, zinc superoxide dismutase (Cu,Zn SOD), catalase (CAT), and glutathione peroxidase (GP), but not manganese superoxide dismutase (Mn SOD), increases in rats during late gestation; the concentrations of Cu,Zn SOD mRNA and CAT mRNA also rise. During early postnatal exposure to > 95% O2, the lung activity of Cu,Zn SOD, CAT, and GP increases. We now show 1) the lung concentration of Mn SOD mRNA and GP mRNA does not increase in late gestation; 2) Mn SOD activity and the concentration of its mRNA and of GP mRNA increase during exposure of neonatal rats to > 95% O2; and 3) as previously shown for CAT mRNA, the increase in lung concentration of the mRNAs for Cu,Zn SOD, Mn SOD, and GP during early postnatal hyperoxia occurs with a 70–80% prolongation of the half-life of these mRNAs. We conclude that 1) in late gestation the level at which lung AOE gene expression is regulated differs among the enzymes, 2) the level at which lung AOE gene expression is regulated shortly after birth in response to > 95% O2 is uniform among the enzymes, and 3) the lung's AOE response to neonatal hyperoxia is not merely a step-up of its prenatal regulation but involves different regulatory mechanisms based on increased stability of AOE mRNAs

scholarly journals Exercise Provides Direct Biphasic Cardioprotection via Manganese Superoxide Dismutase Activation

1999 ◽  
Vol 189 (11) ◽  
pp. 1699-1706 ◽  
Author(s):  
Nobushige Yamashita ◽  
Shiro Hoshida ◽  
Kinya Otsu ◽  
Michio Asahi ◽  
Tsunehiko Kuzuya ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Neutralizing Antibodies ◽  
Time Course ◽  
Manganese Superoxide Dismutase ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Sod Activity ◽  
Manganese Superoxide ◽  
Tnf Α ◽  
Exercise Induced

Epidemiologic investigations have shown that exercise reduces morbidity and mortality from coronary artery disease. In this study, using a rat model, we attempted to determine whether exercise can reduce ischemic injury to the heart and elucidate a mechanism for the cardioprotective effect of exercise. Results showed that exercise significantly reduced the magnitude of a myocardial infarction in biphasic manner. The time course for cardioprotection resembled that of the change in manganese superoxide dismutase (Mn-SOD) activity. The administration of the antisense oligodeoxyribonucleotide to Mn-SOD abolished the expected decrease in infarct size. We showed that the level of tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β) increased after exercise. The simultaneous administration of the neutralizing antibodies to the cytokines abolished the exercise-induced cardioprotection and the activation of Mn-SOD. Furthermore, TNF-α can mimic the biphasic pattern of cardioprotection and activation of Mn-SOD. An antioxidant completely abolished cardioprotection and the activation of Mn-SOD by exercise or the injection of TNF-α as well as exercise-induced increase in TNF-α and IL-1β. The production of reactive oxygen species and endogenous TNF-α and IL-1β induced by exercise leads to the activation of Mn-SOD, which plays major roles in the acquisition of biphasic cardioprotection against ischemia/reperfusion injury in rats.

Inconsistency between manganese superoxide dismutase expression and its activity involved in the degeneration of recognition function induced by chronic aluminum overloading in mice

2015 ◽  
Vol 35 (1) ◽  
pp. 63-68 ◽  
Author(s):  
H-M Qiu ◽  
J-X Yang ◽  
Q-S Jiang ◽  
D He ◽  
Q-X Zhou
Keyword(s):  
Superoxide Dismutase ◽  
Learning And Memory ◽  
Time Course ◽  
Manganese Superoxide Dismutase ◽  
Memory Function ◽  
Sod Activity ◽  
Passive Learning ◽  
Manganese Superoxide ◽  
Recognition Function ◽  
Spatial Recognition

Manganese (Mn) superoxide dismutase (SOD) is mainly located in mitochondrial matrix and is responsible for scavenging about 80% free radicals from oxidative and phospharylative process in mitochondria. It was reported that the insufficiency of Mn SOD expression or activity was connected to the development of neurodegenerative diseases. In this article, we investigated the time course related to the changes of Mn SOD expression and its activity from mouse brain as well as the recognition dysfunction in chronic aluminum (Al) overloading mice. Aluminum gluconate solution (equal to Al 400 mg/kg) was given to mice once a day, 6 days per week for 12 weeks via intragastric gavage. The learning and memory function, malondialdehyde (MDA) level as well as expression and activity of Mn SOD in cortex were determined. It was found that function of passive learning and memory and spatial recognition decreased, MDA level and Mn SOD expression increased during the period of chronic Al loading, but the Mn SOD activity rose from the 4th week and then decreased from the 8th week in cortex in Al overloading mice compared with the control. The results indicated that the inconsistency between Mn SOD expression and its activity might contribute to the development of recognition dysfunction induced by chronic Al overload.

scholarly journals SUPPRESSION OF MANGANESE SUPEROXIDE DISMUTASE ACTIVITY IN ROTENONE-TREATED HUMAN GLIOBLASTOMA T98G CELLS REDUCES CELL VIABILITY

2018 ◽  
Vol 11 (1) ◽  
pp. 48
Author(s):  
Septelia Inawati Wanandi ◽  
Novi Silvia Hardiany ◽  
Nurjati Chairani Siregar ◽  
Mohamad Sadikin
Keyword(s):  
Superoxide Dismutase ◽  
Cell Viability ◽  
Manganese Superoxide Dismutase ◽  
Specific Activity ◽  
High Dose ◽  
Human Glioblastoma ◽  
Manganese Superoxide ◽  
Rotenone Treatment ◽  
Intracellular Ros

  Objective: Glioma is the most common human primary brain tumor which is highly resistant to oxidative stress-based anticancer. The aim of this study was to analyze the effect of rotenone-induced reactive oxygen species (ROS) on the modulation of manganese superoxide dismutase (MnSOD) expression and cell viability in human glioblastoma (GBM) T98G cells.Methods: In this in vitro experimental study, T98G cells were treated with high-dose rotenone (0.5, 5, and 50 μM, respectively). Following rotenone treatment and intracellular ROS, both peroxide and superoxide radicals were determined. Moreover, we analyzed MnSOD mRNA expression, protein, and specific activity, as well as cell survival including viability, proliferation, apoptosis, and mitochondrial structure.Results: High-dose rotenone treatment of T98G cells significantly increased intracellular ROS and MnSOD mRNA, but its protein and specific activity definitely decreased. The treatment also led to a reduction of cell viability, enhancement of apoptosis, and disruption of mitochondrial integrity.Conclusion: Overproduction of ROS in rotenone-treated human GBM T98G cells could suppress the MnSOD protein level and activity even though mRNA synthesis has been increased. This modulation led to reduced survival of T98G cells through induction of cell death rather than inhibition of cell proliferation.

scholarly journals The suppression of manganese superoxide dismutase decreased the survival of human glioblastoma multiforme T98G cells

2017 ◽  
Vol 26 (1) ◽  
pp. 19-25 ◽  
Author(s):  
Novi S. Hardiany ◽  
Mohamad Sadikin ◽  
Nurjati Siregar ◽  
Septelia I. Wanandi
Keyword(s):  
Hydrogen Peroxide ◽  
Superoxide Dismutase ◽  
Glioblastoma Multiforme ◽  
Manganese Superoxide Dismutase ◽  
Superoxide Radical ◽  
Specific Activity ◽  
Human Glioblastoma Multiforme ◽  
Manganese Superoxide ◽  
In Vitro Transfection

Background: Glioblastoma multiforme (GBM) is a primary malignant brain tumor which has poor prognosis. High incidence of oxidative stress-based therapy resistance could be related to the high antioxidant status of GBM cells. Our previous study has reported that manganese superoxide dismutase (MnSOD) antioxidant expression was significantly higher in high grade glioma than in low grade. The aim of this study was to analyze the impact of MnSOD suppression toward GBM cell survival.Methods: This study is an experimental study using human glioblastoma multiforme T98G cell line. Suppression of MnSOD expression was performed using in vitro transfection MnSOD-siRNA. The MnSOD expression was analyzed by measuring the mRNA using real time RT-PCR, protein using ELISA technique, and specific activity of enzyme using inhibition of xantine oxidase. Concentration of reactive oxygen species (ROS) intracellular was determined by measuring superoxide radical and hydrogen peroxide. Cell survival was analyzed by measuring viability, proliferation, and cell apoptosis.Results: In vitro transfection of MnSOD-siRNA suppressed the mRNA, protein, and specific activity of MnSOD. This treatment significantly increased the concentration of superoxide radical; however, it did not influence the concentration of hydrogen peroxide. Moreover, viability MnSOD-suppressing cell significantly decreased, accompanied by increase of cell apoptosis without affecting cell proliferation.Conclusion: The suppression of MnSOD expression leads to decrease glioblastoma multiforme cell survival, which was associated to the increase of cell apoptotic.

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