2048 Prevention of irradiation-induced apoptosis in human esophagus sections in vitro by overexpression of the manganese superoxide dismutase transgene

Author(s):  
J.A. Bray ◽  
M.W. Epperly ◽  
S. Defillipi ◽  
G. Koe ◽  
D. Liggitt ◽  
...  
1994 ◽  
Vol 180 (5) ◽  
pp. 1995-1998 ◽  
Author(s):  
K Ritter ◽  
R J Kühl ◽  
F Semrau ◽  
H Eiffert ◽  
H D Kratzin ◽  
...  

Antibodies directed against the autoantigen p26 were detected in sera from 32 patients with acute Epstein-Barr virus (EBV) infection and clinical symptoms of infectious mononucleosis. P26 has now been identified as the enzyme manganese superoxide dismutase (MnSOD) by comparison of the NH2-terminal amino acid sequence. Antibodies against MnSOD belong to the immunoglobulin class M. They are not detectable in sera of patients with other herpesvirus infections. In the 32 patients investigated, the rise and fall of the autoantibodies coincides with the clinical symptoms. In vitro, the autoantibodies were shown to inhibit the dismutation of superoxide radicals by blocking MnSOD. As presented in the discussion this effect may contribute to the pathogenesis of acute EBV infection.


2006 ◽  
Vol 8 (7-8) ◽  
pp. 1295-1305 ◽  
Author(s):  
Jaya Dasgupta ◽  
Sita Subbaram ◽  
Kip M. Connor ◽  
Ana M. Rodriguez ◽  
Oren Tirosh ◽  
...  

2008 ◽  
Vol 19 (8) ◽  
pp. 820-826 ◽  
Author(s):  
Xichen Zhang ◽  
Michael W. Epperly ◽  
Mark A. Kay ◽  
Zhi-Ying Chen ◽  
Tracy Dixon ◽  
...  

2003 ◽  
Vol 786 (1-2) ◽  
pp. 137-142
Author(s):  
Michael Kleines ◽  
Martin Nellessen ◽  
Lars Schaade ◽  
Klaus Ritter

2021 ◽  
Vol 8 ◽  
Author(s):  
Chong Li ◽  
Yang Fan ◽  
Shuang Li ◽  
Xianrong Zhou ◽  
Kun-Young Park ◽  
...  

The antioxidant effect of soymilk fermented by Lactobacillus plantarum HFY01 (screened from yak yogurt) was investigated on mice with premature aging induced by D-galactose. In vitro antioxidant results showed that L. plantarum HFY01-fermented soymilk (LP-HFY01-DR) had better ability to scavenge the free radicals 1,1-diphenyl-2-picrylhydrazyl (DPPH) and 2,2′-azino-bis (3-ethylbenzthiazoline-6-sulphonic acid) diammonium salt (ABTS) than unfermented soymilk and Lactobacillus bulgaricus-fermented soymilk. Histopathological observation showed that LP-HFY01-DR could protect the skin, spleen and liver, reduce oxidative damage and inflammation. Biochemical results showed that LP-HFY01-DR could effectively upregulate glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) levels and decrease malondialdehyde (MDA) content in the liver, brain, and serum. Real-time quantitative reverse transcription polymerase chain reaction further showed that LP-HFY01-DR could promote the relative expression levels of the genes encoding for cuprozinc superoxide dismutase (Cu/Zn-SOD, SOD1), manganese superoxide dismutase (Mn-SOD, SOD2), CAT, GSH, and GSH-Px in the liver, spleen, and skin. High-performance liquid chromatography results revealed daidzin, glycitin, genistin, daidzein, glycitein, and genistein in LP-HFY01-DR. In conclusion, LP-HFY01-DR could improve the antioxidant capacity in mice with premature aging induced by D-galactose.


Author(s):  
Septelia Inawati Wanandi ◽  
Novi Silvia Hardiany ◽  
Nurjati Chairani Siregar ◽  
Mohamad Sadikin

  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.


2017 ◽  
Vol 26 (1) ◽  
pp. 19-25 ◽  
Author(s):  
Novi S. Hardiany ◽  
Mohamad Sadikin ◽  
Nurjati Siregar ◽  
Septelia I. Wanandi

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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