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M9650016.TXT
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1996-03-09
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Document 0016
DOCN M9650016
TI Inhibition of NF-kappa B activation in human T-cell lines by
anetholdithiolthione.
DT 9605
AU Sen CK; Traber KE; Packer L; Department of Molecular & Cell Biology,
University of; California-Berkeley 94720-3200, USA.
SO Biochem Biophys Res Commun. 1996 Jan 5;218(1):148-53. Unique Identifier
: AIDSLINE MED/96136291
AB Nuclear factor (NF)-kappa B is a redox sensitive cytosolic transcription
factor. Redox regulation of NF-kappa B has been implicated in the
activation of the human immuno-deficiency virus (HIV). Therefore,
inhibition of NF-kappa B activation may be an effective strategy for
acquired immunodeficiency syndrome therapy. Anetholdithiolthione (ADT,
5-[p-methoxyphenyl]-3H-1,2-dithiol-3-thione) is an antioxidant which has
been used to protect against acetaminophen- and CCl4-induced
hepatotoxicity, lipid peroxidation, radiation injury, and also has been
used clinically as an anti-choleretic agent. The present study examined
the effect of ADT pretreatment on NF-kappa B activation in response to a
variety of stimuli such as H2O2, phorbol myristate acetate (PMA) or
tumor necrosis factor alpha (TNF alpha). PMA and TNF alpha induced
activation of (NF)-kappa B in human Jurkat T-cells was partially
inhibited by ADT (0.1 mM) pretreatment. ADT (0.1 mM) also inhibited H2O2
induced activation of the transcription factor in the peroxide sensitive
human Wurzburg T-cells. Furthermore, ADT treated Wurzburg cells had
significantly higher glutathione levels as compared with untreated
cells. H2O2 induced lipid peroxidation in Wurzburg cells was remarkably
inhibited by ADT pretreatment. ADT, a pro-glutathione antioxidant, was
observed to be capable of modulating NF-kappa B activation.
DE Anethole Trithione/*PHARMACOLOGY Cell Line Cell Nucleus/METABOLISM
Human Hydrogen Peroxide/PHARMACOLOGY Kinetics Lymphoma, T-Cell
NF-kappa B/ANTAGONISTS & INHIB/ISOLATION & PURIF/*METABOLISM
T-Lymphocytes Tetradecanoylphorbol Acetate/PHARMACOLOGY Tumor Cells,
Cultured Tumor Necrosis Factor/PHARMACOLOGY JOURNAL ARTICLE
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).