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Redox status of cells influences constitutive or induced NF-kappa B translocation and HIV long terminal repeat activity in human T and monocytic cell lines.
J Immunol 1992; 149(10):3386-93JI

Abstract

We have tested the hypothesis that cellular activation events occurring in T lymphocytes and monocytes and mediated through translocation of the transcription factor NF-kappa B are dependent upon the constitutive redox status of these cells. We used phenolic, lipid-soluble, chain-breaking antioxidants (butylated hydroxyanisole (BHA), nordihydroquairetic acid, or alpha-tocopherol (vitamin E) to show that peroxyl radical scavenging in unstimulated and PMA- or TNF-stimulated cells blocks the functions depending on NF-kappa B activation. BHA was found to suppress not only PMA- or TNF-induced, but also constitutive, HIV-enhancer activity concomitant to an inhibition of NF-kappa B binding activity in both lymphoblastoid T (J.Jhan) and monocytic (U937) cell lines. This was also true for KBF (p50 homodimer) binding activity in U937 cells. Secretion of TNF, the product of another NF-kappa B-dependent gene, was abolished by BHA in PMA-stimulated U937 cells. The anti-oxidative effect of BHA was accompanied by an increase in thiol, but not glutathione, content in stimulated and unstimulated T cell, whereas TNF stimulation itself barely modified the cellular thiol level. Oxidative stress obtained by the addition of H2O2 to the culture medium of J.Jhan or U937 cells could not by itself induce NF-kappa B activation. These observations suggest that TNF and PMA do not lead to NF-kappa B activation through induction of changes in the cell redox status. Rather, TNF and PMA can exert their effect only if cells are in an appropriate redox status, because prior modification toward reduction with BHA treatment prevents this activation. It appears that a basal redox equilibrium tending toward oxidation is a prerequisite for full activation of transduction pathways regulating the activity of NF-kappa B-dependent genes.

Authors+Show Affiliations

Unité d'Immunologie Virale, Institut Pasteur, Paris, France.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

1431113

Citation

Israël, N, et al. "Redox Status of Cells Influences Constitutive or Induced NF-kappa B Translocation and HIV Long Terminal Repeat Activity in Human T and Monocytic Cell Lines." Journal of Immunology (Baltimore, Md. : 1950), vol. 149, no. 10, 1992, pp. 3386-93.
Israël N, Gougerot-Pocidalo MA, Aillet F, et al. Redox status of cells influences constitutive or induced NF-kappa B translocation and HIV long terminal repeat activity in human T and monocytic cell lines. J Immunol. 1992;149(10):3386-93.
Israël, N., Gougerot-Pocidalo, M. A., Aillet, F., & Virelizier, J. L. (1992). Redox status of cells influences constitutive or induced NF-kappa B translocation and HIV long terminal repeat activity in human T and monocytic cell lines. Journal of Immunology (Baltimore, Md. : 1950), 149(10), pp. 3386-93.
Israël N, et al. Redox Status of Cells Influences Constitutive or Induced NF-kappa B Translocation and HIV Long Terminal Repeat Activity in Human T and Monocytic Cell Lines. J Immunol. 1992 Nov 15;149(10):3386-93. PubMed PMID: 1431113.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Redox status of cells influences constitutive or induced NF-kappa B translocation and HIV long terminal repeat activity in human T and monocytic cell lines. AU - Israël,N, AU - Gougerot-Pocidalo,M A, AU - Aillet,F, AU - Virelizier,J L, PY - 1992/11/15/pubmed PY - 1992/11/15/medline PY - 1992/11/15/entrez SP - 3386 EP - 93 JF - Journal of immunology (Baltimore, Md. : 1950) JO - J. Immunol. VL - 149 IS - 10 N2 - We have tested the hypothesis that cellular activation events occurring in T lymphocytes and monocytes and mediated through translocation of the transcription factor NF-kappa B are dependent upon the constitutive redox status of these cells. We used phenolic, lipid-soluble, chain-breaking antioxidants (butylated hydroxyanisole (BHA), nordihydroquairetic acid, or alpha-tocopherol (vitamin E) to show that peroxyl radical scavenging in unstimulated and PMA- or TNF-stimulated cells blocks the functions depending on NF-kappa B activation. BHA was found to suppress not only PMA- or TNF-induced, but also constitutive, HIV-enhancer activity concomitant to an inhibition of NF-kappa B binding activity in both lymphoblastoid T (J.Jhan) and monocytic (U937) cell lines. This was also true for KBF (p50 homodimer) binding activity in U937 cells. Secretion of TNF, the product of another NF-kappa B-dependent gene, was abolished by BHA in PMA-stimulated U937 cells. The anti-oxidative effect of BHA was accompanied by an increase in thiol, but not glutathione, content in stimulated and unstimulated T cell, whereas TNF stimulation itself barely modified the cellular thiol level. Oxidative stress obtained by the addition of H2O2 to the culture medium of J.Jhan or U937 cells could not by itself induce NF-kappa B activation. These observations suggest that TNF and PMA do not lead to NF-kappa B activation through induction of changes in the cell redox status. Rather, TNF and PMA can exert their effect only if cells are in an appropriate redox status, because prior modification toward reduction with BHA treatment prevents this activation. It appears that a basal redox equilibrium tending toward oxidation is a prerequisite for full activation of transduction pathways regulating the activity of NF-kappa B-dependent genes. SN - 0022-1767 UR - https://www.unboundmedicine.com/medline/citation/1431113/Redox_status_of_cells_influences_constitutive_or_induced_NF_kappa_B_translocation_and_HIV_long_terminal_repeat_activity_in_human_T_and_monocytic_cell_lines_ L2 - http://www.jimmunol.org/cgi/pmidlookup?view=long&pmid=1431113 DB - PRIME DP - Unbound Medicine ER -