scholarly journals Lack of p53 Decreases Basal Oxidative Stress Levels in the Brain Through Upregulation of Thioredoxin-1, Biliverdin Reductase-A, Manganese Superoxide Dismutase, and Nuclear Factor Kappa-B

2012 ◽  
Vol 16 (12) ◽  
pp. 1407-1420 ◽  
Author(s):  
Eugenio Barone ◽  
Giovanna Cenini ◽  
Rukhsana Sultana ◽  
Fabio Di Domenico ◽  
Ada Fiorini ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Manganese Superoxide Dismutase ◽  
Nuclear Factor Kappa B ◽  
Nuclear Factor ◽  
Biliverdin Reductase ◽  
Nuclear Factor Kappa ◽  
Manganese Superoxide ◽  
Thioredoxin 1 ◽  
The Brain

scholarly journals Radon inhalation induces manganese-superoxide dismutase in mouse brain via nuclear factor-κB activation

2017 ◽  
Vol 58 (6) ◽  
pp. 887-893 ◽  
Author(s):  
Takahiro Kataoka ◽  
Reo Etani ◽  
Norie Kanzaki ◽  
Yusuke Kobashi ◽  
Yuto Yunoki ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Mouse Brain ◽  
Manganese Superoxide Dismutase ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Ataxia Telangiectasia Mutated ◽  
Sod Activity ◽  
Manganese Superoxide ◽  
Radon Inhalation ◽  
The Brain

Abstract Although radon inhalation increases superoxide dismutase (SOD) activities in mouse organs, the mechanisms and pathways have not yet been fully clarified. The aim of this study was to determine the details of SOD activation in mouse brain tissue following the inhalation of radon at concentrations of 500 or 2000 Bq/m3 for 24 h. After inhalation, brains were removed quickly for analysis. Radon inhalation increased the manganese (Mn)-SOD level and mitochondrial SOD activity. However, the differences were not significant. There were no changes in the Cu/Zn-SOD level or cytosolic SOD activity. Radon inhalation increased the brain nuclear factor (NF)-κB content, which regulates the induction of Mn-SOD, in the nuclear and cytosolic compartments. The level of inhibitor of nuclear factor κB kinase subunit β (IKK-β), which activates NF-κB, was slightly increased by radon inhalation. The expression of cytoplasmic ataxia-telangiectasia mutated kinase in mice inhaling radon at 500 Bq/m3 was 50% higher than in control mice. In addition, NF-κB–inducing kinase was slightly increased after inhaling radon at 2000 Bq/m3. These findings suggest that radon inhalation might induce Mn-SOD protein via NF-κB activation that occurs in response to DNA damage and oxidative stress.

scholarly journals Brain angiotensin or nuclear factor kappa B blockade attenuates cytokines, oxidative stress and decreases sympathoexcitation in hypertension

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Yu‐Ming Kang ◽  
Ying Ma ◽  
Srinivas Sriramula ◽  
Jin‐Ping Zheng ◽  
Zhi‐Ming Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nuclear Factor Kappa B ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa

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.

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