scholarly journals 1087. Effect of the Overexpression of Human Manganese Superoxide Dismutase (hMnSOD) on the Irradiation Resistance of a Rat Submandibular Epithelial Cell Line

2003 ◽  
Vol 7 (5) ◽  
pp. S419
Keyword(s):  
Superoxide Dismutase ◽  
Epithelial Cell ◽  
Cell Line ◽  
Manganese Superoxide Dismutase ◽  
Epithelial Cell Line ◽  
Manganese Superoxide ◽  
Irradiation Resistance

The effect of tumor necrosis factor-α on human malignant glial cells

1992 ◽  
Vol 76 (4) ◽  
pp. 652-659 ◽  
Author(s):  
Rolando F. Del Maestro ◽  
Monica Lopez-Torres ◽  
Warren B. McDonald ◽  
Eric C. Stroude ◽  
Indrasen S. Vaithilingam
Keyword(s):  
Superoxide Dismutase ◽  
Tumor Necrosis Factor ◽  
Cell Line ◽  
Tumor Necrosis ◽  
Manganese Superoxide Dismutase ◽  
Tumor Necrosis Factor Α ◽  
Superoxide Dismutase Activity ◽  
Manganese Superoxide ◽  
Factor Α ◽  
Necrosis Factor

✓ The influence of human recombinant tumor necrosis factor-α has been assessed on a cell line (U-251) derived from a human malignant glial tumor. The results of this study demonstrate that tumor necrosis factor-α at doses of 50 and 100 ng/ml: 1) did not have cytotoxic or cytostatic effects on the U-251 cell line; 2) significantly increased the intracellular activity of manganese superoxide dismutase but had no effect on copper and zinc superoxide dismutase, catalase, or glutathione peroxidase activity; and 3) did not significantly alter the intracellular or extracellular general protease and collagenase type IV activity of these cells. The resistance of the U-251 cell line to tumor necrosis factor-α cytotoxicity may be related in part to the high intrinsic manganese superoxide dismutase activity present in this cell line combined with the ability of this cell line to induce substantial amounts of protective manganese superoxide dismutase activity in response to tumor necrosis factor-α.

scholarly journals Tumor suppressive activity of a variant isoform of manganese superoxide dismutase released by a human liposarcoma cell line

2006 ◽  
Vol 119 (4) ◽  
pp. 932-943 ◽  
Author(s):  
Aldo Mancini ◽  
Antonella Borrelli ◽  
Antonella Schiattarella ◽  
Stefania Fasano ◽  
Antonella Occhiello ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Cell Line ◽  
Manganese Superoxide Dismutase ◽  
Suppressive Activity ◽  
Manganese Superoxide

scholarly journals A role for manganese superoxide dismutase in radioprotection of hematopoietic stem cells by interleukin-1

Blood ◽  
1993 ◽  
Vol 81 (3) ◽  
pp. 639-646
Author(s):  
J Eastgate ◽  
J Moreb ◽  
HS Nick ◽  
K Suzuki ◽  
N Taniguchi ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Superoxide Dismutase ◽  
Antioxidant Enzyme ◽  
Cell Line ◽  
Manganese Superoxide Dismutase ◽  
Bone Marrow Cells ◽  
Interleukin 1 ◽  
Leukemic Cell ◽  
Manganese Superoxide ◽  
Marrow Cells

Pretreatment with interleukin-1 (IL-1) has been shown to protect mice from the myelotoxicity associated with irradiation via a mechanism potentially mediated through the induction of the antioxidant enzyme manganese superoxide dismutase (MnSOD). In this study, we have compared the ability of IL-1 to induce MnSOD mRNA in murine bone marrow cells and human cell lines with its ability to protect these cells against the damaging effects of ionizing radiation. Bone marrow cells obtained from mice 6 hours after a single injection of IL-1 demonstrate a dose- dependent increase in the expression of MnSOD RNA. In this same study, IL-1 was also shown to be radioprotective when given to mice 20 hours before lethal irradiation. Similarly, in vitro treatment with IL-1 of bone marrow cells isolated from 5-fluorouracil-treated mice results in elevated levels of MnSOD RNA. Pretreatment with IL-1 also protected bone marrow long-term culture-initiating cells capable of reconstituting irradiated stromal cultures from an irradiation insult. Furthermore, IL-1-treated human bone marrow cells display both elevated MnSOD RNA and protein levels when compared with media controls. The human A375 melanoma, A549 adenocarcinoma, and factor-dependent TF-1 leukemic cell lines demonstrate low basal MnSOD RNA levels that increase following treatment with IL-1. For the A375 cells, this correlates with increased MnSOD protein expression and radioprotection by IL-1 using a colony assay. In contrast, the chronic myelogenous leukemic cell line, K562, displays a high basal MnSOD RNA level, and this RNA expression is not further increased by IL-1 treatment. In addition, these cells are comparatively radioresistant and are not further protected by IL-1 treatment. Finally, the Mo-7 cell line displays a low basal level of MnSOD RNA that correlates with a high sensitivity to irradiation and IL-1 pretreatment has no effect on MnSOD RNA levels. Our results indicate that increased radioprotection by IL-1 correlates with the induction of the antioxidant enzyme MnSOD and this induction may be an important factor in IL-1 radioprotection.

scholarly journals IκBα (inhibitory κBα) identified as labile repressor of MnSOD (manganese superoxide dismutase) expression

2004 ◽  
Vol 384 (3) ◽  
pp. 543-549 ◽  
Author(s):  
Kelley K. KININGHAM ◽  
Chotiros DAOSUKHO ◽  
Daret K. ST. CLAIR
Keyword(s):  
Superoxide Dismutase ◽  
Cell Line ◽  
Manganese Superoxide Dismutase ◽  
Phorbol Esters ◽  
De Novo ◽  
Nuclear Factor Κb ◽  
Binding Activity ◽  
Inhibitory Protein ◽  
Manganese Superoxide ◽  
Pre Treatment

Cytokines, phorbol esters, radiation and chemotherapeutic drugs up-regulate the expression of MnSOD (manganese superoxide dismutase). Using the VA-13 cell line, we studied the regulation of SOD2 upon treatment with PMA. Pre-treatment with CHX (cycloheximide) followed by PMA led to significantly higher levels of MnSOD mRNA compared with those with either agent alone, suggesting de novo synthesis of an inhibitory protein. PMA treatment modulates redox-sensitive transcription factors, therefore we evaluated the effects of this combination treatment upon AP-1 (activator protein 1) and NF-κB (nuclear factor κB), two trans-acting factors suggested to play a role in SOD2 regulation. Co-administration of CHX and PMA led to a time-dependent increase in the binding activity of NF-κB. Therefore we evaluated IκBα (inhibitory κBα) and found that co-administration decreased its steady-state level compared with either agent alone, suggesting that enhanced NF-κB activation is due to inhibition of IκBα synthesis. PMA activates PKC (protein kinase C) enzymes which phosphorylate IκBα, leading to its degradation, therefore we used GF109203X to inhibit PKC activity. Stable transfection utilizing a PMA-responsive element in the human SOD2 gene, showed a concentration-dependent decrease in luciferase and NF-κB-binding activity with GF109203X. Western blot analysis indicated the presence of several PKC isoforms in the VA-13 cell line; however, PMA pre-treatment specifically down-regulated α and βI, suggesting a role for one or more of these proteins in SOD2 induction. Taken together, these results indicate that the PKC pathway leading to SOD2 induction proceeds at least in part through NF-κB and that inhibition of IκBα synthesis might serve as a potential pharmacological approach to up-regulate MnSOD.

scholarly journals A role for manganese superoxide dismutase in radioprotection of hematopoietic stem cells by interleukin-1

Blood ◽  
1993 ◽  
Vol 81 (3) ◽  
pp. 639-646 ◽  
Author(s):  
J Eastgate ◽  
J Moreb ◽  
HS Nick ◽  
K Suzuki ◽  
N Taniguchi ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Superoxide Dismutase ◽  
Antioxidant Enzyme ◽  
Cell Line ◽  
Manganese Superoxide Dismutase ◽  
Bone Marrow Cells ◽  
Interleukin 1 ◽  
Leukemic Cell ◽  
Manganese Superoxide ◽  
Marrow Cells

Abstract Pretreatment with interleukin-1 (IL-1) has been shown to protect mice from the myelotoxicity associated with irradiation via a mechanism potentially mediated through the induction of the antioxidant enzyme manganese superoxide dismutase (MnSOD). In this study, we have compared the ability of IL-1 to induce MnSOD mRNA in murine bone marrow cells and human cell lines with its ability to protect these cells against the damaging effects of ionizing radiation. Bone marrow cells obtained from mice 6 hours after a single injection of IL-1 demonstrate a dose- dependent increase in the expression of MnSOD RNA. In this same study, IL-1 was also shown to be radioprotective when given to mice 20 hours before lethal irradiation. Similarly, in vitro treatment with IL-1 of bone marrow cells isolated from 5-fluorouracil-treated mice results in elevated levels of MnSOD RNA. Pretreatment with IL-1 also protected bone marrow long-term culture-initiating cells capable of reconstituting irradiated stromal cultures from an irradiation insult. Furthermore, IL-1-treated human bone marrow cells display both elevated MnSOD RNA and protein levels when compared with media controls. The human A375 melanoma, A549 adenocarcinoma, and factor-dependent TF-1 leukemic cell lines demonstrate low basal MnSOD RNA levels that increase following treatment with IL-1. For the A375 cells, this correlates with increased MnSOD protein expression and radioprotection by IL-1 using a colony assay. In contrast, the chronic myelogenous leukemic cell line, K562, displays a high basal MnSOD RNA level, and this RNA expression is not further increased by IL-1 treatment. In addition, these cells are comparatively radioresistant and are not further protected by IL-1 treatment. Finally, the Mo-7 cell line displays a low basal level of MnSOD RNA that correlates with a high sensitivity to irradiation and IL-1 pretreatment has no effect on MnSOD RNA levels. Our results indicate that increased radioprotection by IL-1 correlates with the induction of the antioxidant enzyme MnSOD and this induction may be an important factor in IL-1 radioprotection.

Mesalamine induces manganese superoxide dismutase in rat intestinal epithelial cell lines and in vivo

2001 ◽  
Vol 281 (4) ◽  
pp. G1044-G1050 ◽  
Author(s):  
J. F. Valentine
Keyword(s):  
Superoxide Dismutase ◽  
Epithelial Cell ◽  
Cell Lines ◽  
Intestinal Epithelial Cell ◽  
Manganese Superoxide Dismutase ◽  
Mrna Levels ◽  
Intestinal Epithelial ◽  
Manganese Superoxide ◽  
Epithelial Cell Lines

Mesalamine (5-ASA) is effective in the treatment of inflammatory bowel diseases. However, the mechanisms of action of 5-ASA remain unclear. IEC-6 and IRD-98, nontransformed rat small intestinal epithelial cell lines, were used to examine the effect of 5-ASA on the expression of manganese superoxide dismutase (MnSOD). Rats were given 5-ASA enemas to determine the effect on colonic MnSOD expression. Treatment with 5-ASA at 0.02 or 2 mg/ml induced MnSOD mRNA levels 2.67-fold or 5.66-fold, respectively. Inhibition of 5-lipoxygenase activating protein with MK-886 or cyclooxygenase with indomethacin did not influence the level of MnSOD mRNA. Nuclear run-on experiments demonstrated an increase in de novo transcription following treatment with 5-ASA. MnSOD protein levels were induced 2-fold at 24 h and 4.23-fold at 48 h following treatment with 1 mg/ml 5-ASA. 5-ASA increased MnSOD 1.7-fold in vivo. Pretreatment with 5-ASA significantly protected IRD-98 cells from tumor necrosis factor-α cytotoxicity. This is the first example of transcriptional gene regulation by 5-ASA. The induction of MnSOD by 5-ASA may contribute to the therapeutic mechanism of 5-ASA.

An Established Epithelial Cell Line (NPC/HK1) from a Nasopharyngeal Carcinoma - II. A Sem Study

1982 ◽  
Vol 40 ◽  
pp. 224-225
Author(s):  
Li C.L. ◽  
Chew E.C. ◽  
Huang D.P. ◽  
Ho H.C. ◽  
Mak L.S. ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Epithelial Cell ◽  
Surface Morphology ◽  
Cell Line ◽  
Epithelial Cell Line ◽  
Present Communication ◽  
Cells In Culture ◽  
Sem Study ◽  
Well Differentiated

An epithelial cell line, NPC/HK1, has recently been successfully established from a nasopharyngeal carcinoma of the moderately to well differentiated squamous type. The present communication reports on the surface morphology of the NPC/HK1 cells in culture.

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