UDN glycoprotein regulates activities of manganese-superoxide dismutase, activator protein-1, and nuclear factor-κB stimulated by reactive oxygen radicals in lipopolysaccharide-stimulated HCT-116 cells

Recently, we demonstrated that 3,3′,5-triiodothyronine (T3) induces oxidative stress in rat liver, with enhancement in the DNA binding of nuclear factor-κB (NF-κB) and the NF-κB-dependent expression of tumor necrosis factor-α (TNF-α). In this study, we show that T3 administration (daily doses of 0.1 mg/kg i.p. for three consecutive days) elicited a calorigenic response and higher liver O2 consumption rates, with increased serum levels of TNF-α (ELISA), liver inhibitor of κB (IκB-α) phosphorylation (Western blot analysis), and hepatic NF-κB DNA binding (EMSA) at 56–72 h after treatment. Within this time interval, liver manganese superoxide dismutase (MnSOD) activity and the protein expression of MnSOD and Bcl-2 are enhanced. These changes are abrogated by the administration of α-tocopherol (100 mg/kg i.p.) prior to T3. It is concluded that T3 treatment leads to the redox upregulation of MnSOD and Bcl-2 in rat liver, in association with TNF-α release and activation of the IκB-α kinase/NF-κB cascade, which may constitute a protective mechanism against free radical toxicity involving cell death signaling.

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Nuclear factor-κB dependency of doxorubicin sensitivity in gastric cancer cells is determined by manganese superoxide dismutase expression

Cancer Science ◽

10.1111/j.1349-7006.2008.00789.x ◽

2008 ◽

Vol 99 (6) ◽

pp. 1117-1124 ◽

Cited By ~ 22

Author(s):

Sung Jin Cho ◽

Jong-Wan Park ◽

Jae Seung Kang ◽

Woo Ho Kim ◽

Yong-Sung Juhnn ◽

...

Keyword(s):

Gastric Cancer ◽

Superoxide Dismutase ◽

Cancer Cells ◽

Manganese Superoxide Dismutase ◽

Nuclear Factor Κb ◽

Nuclear Factor ◽

Gastric Cancer Cells ◽

Manganese Superoxide

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

Journal of Radiation Research ◽

10.1093/jrr/rrx048 ◽

2017 ◽

Vol 58 (6) ◽

pp. 887-893 ◽

Cited By ~ 3

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.

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Nuclear factor κB-dependent mechanisms coordinate the synergistic effect of PMA and cytokines on the induction of superoxide dismutase 2

Biochemical Journal ◽

10.1042/bj3530147 ◽

2000 ◽

Vol 353 (1) ◽

pp. 147-156 ◽

Cited By ~ 37

Author(s):

Kelley K. KININGHAM ◽

Yong XU ◽

Chotiros DAOSUKHO ◽

Bilyana POPOVA ◽

Daret K. ST CLAIR

Keyword(s):

Superoxide Dismutase ◽

Manganese Superoxide Dismutase ◽

Simian Virus 40 ◽

Fibroblast Cell ◽

Nuclear Factor Κb ◽

Simian Virus ◽

Physical Interaction ◽

Nuclear Factor ◽

Simultaneous Treatment ◽

Radiation Chemical

Manganese superoxide dismutase (MnSOD) serves a protective role under conditions of oxidative stress mediated by such diverse agents as adriamycin, radiation, chemical hypoxia and ischaemia and might act as a newly recognized type of tumour-suppressor. MnSOD is an inducible enzyme; however, the signalling molecules and pathways involved in its induction have not been fully elucidated. Recently we reported the identification of a 342bp enhancer within the second intron (I2E) of the human gene encoding MnSOD (SOD2), which contains sites for binding nuclear factor κB (NF-κB), CCAAT-enhancer-binding protein (C/EBP) and nuclear factor 1 (NF-1). Using a human fibroblast cell line transformed by simian virus 40, we have identified the I2E fragment as being responsive to PMA. Furthermore, simultaneous treatment with PMA and cytokines (tumour necrosis factor α and interleukin 1β) synergistically increases MnSOD induction. The use of mutant constructs identified the NF-κB element within the enhancer fragment as being essential for the PMA and PMA/cytokine effect. Mutations in the C/EBP- and NF-1-binding sites revealed a potential co-operation between proteins that bind to these sites and the NF-κB element. Evaluation of inhibitory κB (IκB)-α and IκB-β proteins reveals agent-specific differences in their turnover kinetics. Both C/EBP and NF-κB DNA-binding activities were increased in cells receiving a combination of cytokine and PMA. Supershift and immunoprecipitation studies suggest a physical interaction between C/EBP and NF-κB proteins. Taken together, these studies suggest the activation of multiple transcription factors as well as pathways leading to increased NF-κB activity as being the mechanisms responsible for the synergistic induction of MnSOD by PMA and cytokines.

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