| Name | tumor necrosis factor alpha |
|---|---|
| Synonyms | Cachectin; DIF; TNF; TNF alpha; TNF a; TNFA; TNFSF 2; TNFSF2… |
| Name | sodium arsenite |
|---|---|
| CAS | sodium arsenenite |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 7743356 | Abello PA, Buchman TG: Heat shock-induced cell death in murine microvascular endothelial cells depends on priming with tumor necrosis factor-alpha or interferon-gamma. Shock. 1994 Nov;2(5):320-3. When these endothelial cells were treated first with tumor necrosis factor-alpha followed by induction of the heat shock response with either heat or sodium arsenite (As), a standard chemical inducer of the heat shock response in vitro, a tumor necrosis factor dose-dependent cytotoxicity was observed, similar to that which we had seen previously in porcine endothelial cells primed with LPS. |
7(0,0,1,2) | Details |
| 8946648 | Wang JH, Redmond HP, Watson RW, Condron C, Bouchier-Hayes D: The beneficial effect of on the prevention of human endothelial cell death. Shock. 1996 Nov;6(5):331-8. Sodium arsenite (80 microM) alone and in combination with tumor necrosis factor-alpha (25 ng/mL) caused EC apoptosis after 24 h of treatment. |
7(0,0,1,2) | Details |
| 15797874 | Zhang N, Ahsan MH, Zhu L, Sambucetti LC, Purchio AF, West DB: NF-kappaB and not the MAPK signaling pathway regulates GADD45beta expression during acute inflammation. J Biol Chem. 2005 Jun 3;280(22):21400-8. Epub 2005 Mar 29. We found that a number of agents that induce oxidative stress, such as sodium arsenite, CCl4, lipopolysaccharide (LPS), or tumor necrosis factor-alpha, are able to induce luciferase expression throughout the entire animal. |
6(0,0,1,1) | Details |
| 17224793 | Wang Q, Guo XL, Noel G, Ogle C: Heat shock stress ameliorates cytokine mixture-induced permeability by downregulating the and signal transducer and activator of transcription pathways in Caco-2 cells. Shock. 2007 Feb;27(2):179-85. A monolayer of Caco-2 cells were pretreated with sodium arsenite (SA, 500 micromol/L) for 1 h, followed by a 1-h recovery, and then stimulated with a cytokine mixture (cytomix: tumor necrosis factor alpha [10 ng/mL], interferon beta [1000 U/mL], and interleukin [IL] 1beta [1 ng/mL]) for 24 h. |
6(0,0,1,1) | Details |
| 7653571 | Wang JH, Redmond HP, Watson RW, Bouchier-Hayes D: Role of lipopolysaccharide and tumor necrosis factor-alpha in induction of hepatocyte necrosis. Am J Physiol. 1995 Aug;269(2 Pt 1):G297-304. However, LPS and TNF-alpha, in the presence of sodium arsenite (a heat shock inducer), were unable to induce HC apoptosis. |
2(0,0,0,2) | Details |
| 9548797 | Sakurai T, Kaise T, Matsubara C: Inorganic and methylated arsenic compounds induce cell death in murine macrophages via different mechanisms. Chem Res Toxicol. 1998 Apr;11(4):273-83. The inorganic arsenicals also induced marked release of an inflammatory cytokine, tumor necrosis factor alpha (TNF alpha), at cytotoxic doses. |
2(0,0,0,2) | Details |
| 7851416 | Huot J, Lambert H, Lavoie JN, Guimond A, Houle F, Landry J: Characterization of 45-kDa/54-kDa HSP27 kinase, a stress-sensitive kinase which may activate the phosphorylation-dependent protective function of mammalian 27-kDa heat-shock protein HSP27. Eur J Biochem. 1995 Jan 15;227(1-2):416-27. Here we investigated comparatively the mechanisms of HSP27 phosphorylation by oxidative stresses, exposures to tumor necrosis factor (TNF), heat shock and growth factors. The kinase activity in extracts of cells stimulated by heat shock, H2O2, sodium arsenite, TNF or growth factors was identified by in-gel renaturation and purified approximately 8000-fold by sequential chromatography. |
1(0,0,0,1) | Details |
| 15551947 | Di Giampaolo L, Di Gioacchino M, Qiao N, Travaglini P, D'Intino A, Kouri M, Ponti J, Castellani ML, Reale M, Gabriele E, Boscolo P: "In vitro" effects of different arsenic compounds on PBMC (preliminary study). G Ital Med Lav Ergon. 2004 Jul-Sep;26(3):183-6. Aim of this investigation was to compare the effects of 10 (-4) M and 10 (-7) M As compounds on spontaneous and PHA stimulated PBMC proliferation and IFN-gamma and TNF-alpha release. The inhibitory effect of the 10 (-4) M As salts was in the following order: momo-methyl-arsinous acic (MMAs (III)) > sodium arsenite (As (III)) > tetraphenyl arsonium (As (V)) > arsenate (As (V)) > - and -esa-fluorum arsenate (As (V)) > dimethyl arsinic acid (DMAs (V)), while monomethyl-arsonic-acid (MMAs (V)) and arsenobetaine did not exert immune effects. 10 (-7) M MMAs (III) stimulated the spontaneous PBMC proliferation, while As (III) and DMAs (V) enhanced the PHA stimulated PBMC proliferation. |
1(0,0,0,1) | Details |
| 16243048 | Sun D, Chen D, Du B, Pan J: Heat shock response inhibits NF-kappaB activation and cytokine production in murine Kupffer cells. J Surg Res. 2005 Nov;129(1):114-21. MATERIALS AND METHODS: Kupffer cells were isolated from mice by collagenase digestion and HSP was induced by culturing Kupffer cells with sodium arsenite. Supernatant tumor necrosis factor (TNF)-alpha, interleukin (IL)-6 and IL-10 levels were measured by ELISA. |
1(0,0,0,1) | Details |
| 17185630 | Kuboki S, Schuster R, Blanchard J, Pritts TA, Wong HR, Lentsch AB: Role of heat shock protein 70 in hepatic ischemia-reperfusion injury in mice. Am J Physiol Gastrointest Liver Physiol. 2007 Apr;292(4):G1141-9. Epub 2006 Dec 21. In addition, arsenite similarly reduced liver neutrophil recruitment and liver nuclear factor-kappaB activation, and attenuated serum levels of tumor necrosis factor-alpha and macrophage inflammatory protein-2, but increased levels of interleukin (IL)-6. To explore the function of HSP70, sodium arsenite (8 mg/kg iv) was injected before surgery. |
1(0,0,0,1) | Details |
| 8903404 | de Vera ME, Kim YM, Wong HR, Wang Q, Billiar TR, Geller DA: Heat shock response inhibits cytokine-inducible synthase expression in rat hepatocytes. Hepatology. 1996 Nov;24(5):1238-45. Sodium arsenite (Ars) or hyperthermia (43 degrees C) induced the synthesis of hsp72 messenger RNA (mRNA) and protein in hepatocytes, indicating activation of the HSR. In the absence of the HSR, combinations of interleukin-1beta (IL-1beta), tumor necrosis factor alpha (TNF-alpha), and interferon gamma (IFN-gamma) stimulated high levels of NOS2 mRNA and (NO) synthesis. |
1(0,0,0,1) | Details |
| 17545621 | Ivanov VN, Zhou H, Hei TK: Sequential treatment by ionizing radiation and sodium arsenite dramatically accelerates TRAIL-mediated apoptosis of human melanoma cells. Cancer Res. 2007 Jun 1;67(11):5397-407. We show in the present study that gamma-irradiation, as well as alpha-particle exposure, dramatically increases the susceptibility of melanoma cells to recombinant tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis via up-regulation of surface TRAIL-receptor 1/receptor 2 (DR4/DR5) levels and to Fas ligand-mediated apoptosis via up-regulation of surface Fas levels. |
1(0,0,0,1) | Details |
| 12842450 | Carter Y, Liu G, Stephens WB, Carter G, Yang J, Mendez C: Heat shock protein (HSP72) and p38 MAPK involvement in sublethal hemorrhage (SLH)-induced tolerance. J Surg Res. 2003 May 1;111(1):70-7. This study investigated if SLH induces in vivo HSP72 expression and whether in vitro HSP72 induction by sodium arsenite (NaArs) alters intracellular signal transduction and cytokine production similar to SLH. Reverse transcription polymerase chain reaction, Western blots, and enzyme-linked immunosorbent assay were performed for gene, MAPK, and protein expression (tumor necrosis factor [TNF], HSP, p38). |
1(0,0,0,1) | Details |
| 11353140 | Liu J, Kadiiska MB, Liu Y, Lu T, Qu W, Waalkes MP: Stress-related gene expression in mice treated with inorganic arsenicals. Toxicol Sci. 2001 Jun;61(2):314-20. Increases in caspase-1 and cytokines such as tumor necrosis factor-alpha (TNF-alpha) and macrophage inflammatory protein-2 were also evident. Mice were injected sc with either sodium arsenite [As (III), 100 micromol/kg], arsenate [As (V), 300 micromol/kg], or saline. |
1(0,0,0,1) | Details |
| 10216529 | Tsuruma T, Yagihashi A, Watanabe N, Yajima T, Kameshima H, Araya J, Hirata K: Heat-shock protein-73 protects against small intestinal warm ischemia-reperfusion injury in the rat. Surgery. 1999 Apr;125(4):385-95. METHODS: Hsp-73 expression was induced in rat small intestine with use of sodium arsenite injected (6 mg/kg) through a catheter cannulated into the left common carotid artery 24 hours before ischemia (group 1). RESULTS: The mean peak plasma levels of tumor necrosis factor-alpha and cytokine-induced neutrophil chemoattractant after reperfusion were lower in group 1 than in group 2. |
1(0,0,0,1) | Details |
| 1730670 | Landry J, Lambert H, Zhou M, Lavoie JN, Hickey E, Weber LA, Anderson CW: Human HSP27 is phosphorylated at serines 78 and 82 by heat shock and mitogen-activated kinases that recognize the same amino acid motif as S6 kinase II. J Biol Chem. 1992 Jan 15;267(2):794-803. Heat shock of HeLa cell cultures, or treatment with arsenite, phorbol ester, or tumor necrosis factor, caused a rapid phosphorylation of preexisting HSP27 and the appearance of three phosphorylated isoforms, HSP27 B, C, and D. |
1(0,0,0,1) | Details |
| 8970379 | Ribeiro SP, Villar J, Downey GP, Edelson JD, Slutsky AS: Effects of the stress response in septic rats and LPS-stimulated alveolar macrophages: evidence for TNF-alpha posttranslational regulation. Am J Respir Crit Care Med. 1996 Dec;154(6 Pt 1):1843-50. We have previously demonstrated that induction of the stress response, by heat stress or sodium arsenite, administered 18 h before initiation of sepsis in rats, significantly decreased mortality and lung injury. As a possible mechanism underlying this effect, we hypothesized that the induction of the stress response, prior to bacterial endotoxin (lipopolysaccharide, LPS) stimulation, would cause a decrease in synthesis and/or release of tumor necrosis factor-alpha (TNF-alpha), making the animals more resistant to sepsis. |
1(0,0,0,1) | Details |
| 12676792 | Mathas S, Lietz A, Janz M, Hinz M, Jundt F, Scheidereit C, Bommert K, Dorken B: Inhibition of NF-kappaB essentially contributes to arsenic-induced apoptosis. Blood. 2003 Aug 1;102(3):1028-34. Epub 2003 Apr 3. Furthermore, arsenic treatment down-regulated NF-kappaB target genes, including tumor necrosis factor-alphareceptor-associated factor 1 (TRAF1), c-IAP2, interleukin-13 (IL-13), and CCR7. |
1(0,0,0,1) | Details |
| 7735982 | Lappas GD, Karl IE, Hotchkiss RS: Effect of and sodium arsenite on HSP-72 formation and on survival in a murine endotoxin model. Shock. 1994 Jul;2(1):34-9; discussion 40. Although the mechanism by which hyperthermia protects is unknown, two possible etiologies are induction of HSPs and/or production of cytokines, interleukin-1 alpha (IL-1 alpha) or tumor necrosis factor-alpha (TNF-alpha). |
1(0,0,0,1) | Details |
| 19083458 | Pai MH, Chien YW, Tsai YH, Hu YM, Yeh SL: reduces the expression of leukocyte integrins leukocyte function-associated antigen-1 and macrophage antigen-1 in mice exposed to arsenic. Nutr Res. 2008 Aug;28(8):544-9. The control group drank deionized water, whereas the experimental group drank deionized water containing 50 ppm of sodium arsenite. |
0(0,0,0,0) | Details |
| 1417842 | Zilli D, Voelkel-Johnson C, Skinner T, Laster SM: The adenovirus E3 region 14.7 kDa protein, heat and sodium arsenite inhibit the TNF-induced release of Biochem Biophys Res Commun. 1992 Oct 15;188(1):177-83. In this report we show that the adenovirus E3 region 14.7 kDa protein, heat and sodium arsenite, which have been defined previously as inhibitors of cytolysis, inhibit the tumor necrosis factor-alpha (TNF)-induced release of 3H- from cycloheximide-sensitized C3HA fibroblasts. |
81(1,1,1,1) | Details |
| 8917704 | Germolec DR, Yoshida T, Gaido K, Wilmer JL, Simeonova PP, Kayama F, Burleson F, Dong W, Lange RW, Luster MI: Arsenic induces overexpression of growth factors in human keratinocytes. . Toxicol Appl Pharmacol. 1996 Nov;141(1):308-18. We observed increased mRNA transcripts and secretion of keratinocyte growth factors, including granulocyte macrophage-colony stimulating factor (GM-CSF) and transforming growth factor-alpha (TGF alpha) and the proinflammatory cytokine tumor necrosis factor-alpha in primary human epidermal keratinocytes cultured in the presence of low micromolar concentrations of sodium arsenite. |
31(0,1,1,1) | Details |
| 9176145 | Wang JH, Redmond HP, Watson RW, Bouchier-Hayes D: Induction of human endothelial cell apoptosis requires both heat shock and oxidative stress responses. Am J Physiol. 1997 May;272(5 Pt 1):C1543-51. In this study we employed the proinflammatory mediators lipopolysaccharide (LPS) and tumor necrosis factor-alpha (TNF-alpha), the chemical reagent sodium arsenite, and heat shock to trigger the stress gene responses. |
31(0,1,1,1) | Details |
| 7541446 | Satoh J, Kim SU: Cytokines and growth factors induce HSP27 phosphorylation in human astrocytes. J Neuropathol Exp Neurol. 1995 Jul;54(4):504-12. The level of HSP27 phosphorylation was elevated greatly after a 30 minute exposure to heat shock, sodium arsenite, interleukin-1 (IL-1 alpha and IL-1 beta), and tumor necrosis factor-alpha (TNF-alpha) with an increased expression of a diphosphorylated "c" isoform. |
31(0,1,1,1) | Details |
| 10779545 | Werz O, Klemm J, Samuelsson B, Radmark O: 5-lipoxygenase is phosphorylated by p38 kinase-dependent MAPKAP kinases. Proc Natl Acad Sci U S A. 2000 May 9;97(10):5261-6. Different agents activated the 5-LO kinase activities, including stimuli for cellular leukotriene biosynthesis (A23187, thapsigargin, N-formyl-leucyl- compounds that up-regulate the capacity for leukotriene biosynthesis (phorbol 12- 13- tumor necrosis factor alpha, granulocyte/macrophage colony-stimulating factor), and well known p38 stimuli as sodium arsenite and |
31(0,1,1,1) | Details |
| 9219559 | Germolec DR, Spalding J, Boorman GA, Wilmer JL, Yoshida T, Simeonova PP, Bruccoleri A, Kayama F, Gaido K, Tennant R, Burleson F, Dong W, Lang RW, Luster MI: Arsenic can mediate skin neoplasia by chronic stimulation of keratinocyte-derived growth factors. Mutat Res. 1997 Jun;386(3):209-18. We observed increased mRNA transcripts and secretion of keratinocyte growth factors, including granulocyte macrophage-colony stimulating factor (GM-CSF) and transforming growth factor-alpha (TGF-alpha) and the proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) in primary human epidermal keratinocytes cultured in the presence of low micromolar concentrations of sodium arsenite. |
31(0,1,1,1) | Details |
| 7982393 | Lantz RC, Parliman G, Chen GJ, Carter DE: Effect of arsenic exposure on alveolar macrophage function. Environ Res. 1994 Nov;67(2):183-95. One day following intratracheal instillation of 1 mg/ml (as arsenic) of either sodium arsenite (As (III)) or arsenate (As (V)), PAM were lavaged and analyzed for alterations in (O2-), and tumor necrosis factor (TNF-alpha) production. |
31(0,1,1,1) | Details |