Document Detail

Inorganic mercury dissociates preassembled Fas/CD95 receptor oligomers in T lymphocytes.
MedLine Citation:
PMID:  16039944     Owner:  NLM     Status:  MEDLINE    
Genetically susceptible rodents exposed to low burdens of inorganic mercury (Hg2+) develop autoimmune disease. Previous studies have shown that low, noncytotoxic levels of Hg2+ inhibit Fas-mediated apoptosis in T cells. These results suggest that inhibition of the Fas death receptor pathway potentially contributes to autoimmune disease after Hg2+ exposure, as a consequence of disruption of peripheral tolerance. The formation of active death inducing signaling complexes (DISC) following CD95/Fas receptor oligomerization is a primary step in the Fas-mediated apoptotic pathway. Other recent studies have shown that Hg2+ at concentrations that inhibit apoptosis also inhibit formation of active DISC, suggesting that inhibition of DISC is the mechanism responsible for Hg2+-mediated inhibition of apotosis. Preassociated Fas receptors have been implicated as key elements necessary for the production of functional DISC. We present evidence in this study showing that low and nontoxic concentrations of Hg2+ induce the dissociation of preassembled Fas receptor complexes in Jurkat T cells. Thus, this Hg2+-induced event should subsequently decrease the amount of preassembled Fas available for DISC formation, potentially resulting in the attenuation of Fas-mediated apoptosis in T lymphocytes.
Stamatina E Ziemba; Michael J McCabe; Allen J Rosenspire
Related Documents :
12672404 - The expression of plasma nucleosomes in mice undergoing in vivo apoptosis.
11675354 - Caspase 8 activation independent of fas (cd95/apo-1) signaling may mediate killing of b...
10329044 - Nitric oxide sensitizes ovarian tumor cells to fas-induced apoptosis.
16039944 - Inorganic mercury dissociates preassembled fas/cd95 receptor oligomers in t lymphocytes.
16299714 - Aberrant cellular immune responses in humans infected persistently with parvovirus b19.
15163104 - Impact of nutritional status and nutrient supplements on immune responses and incidence...
Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.     Date:  2005-01-08
Journal Detail:
Title:  Toxicology and applied pharmacology     Volume:  206     ISSN:  0041-008X     ISO Abbreviation:  Toxicol. Appl. Pharmacol.     Publication Date:  2005 Aug 
Date Detail:
Created Date:  2005-07-25     Completed Date:  2005-09-15     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0416575     Medline TA:  Toxicol Appl Pharmacol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  334-42     Citation Subset:  IM    
Department of Biological Sciences, Wayne State University, 5047 Gullen Mall, Detroit, MI 48202, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Antigens, CD95 / metabolism*
Blotting, Western
Chlorides / pharmacology
Death Domain Receptor Signaling Adaptor Proteins
Electrophoresis, Polyacrylamide Gel
Environmental Pollutants / toxicity*
Jurkat Cells
Mercuric Chloride / toxicity*
Receptors, Tumor Necrosis Factor / metabolism
T-Lymphocytes / drug effects*,  metabolism
Zinc Compounds / pharmacology
Grant Support
Reg. No./Substance:
0/Antigens, CD95; 0/Biopolymers; 0/Chlorides; 0/Death Domain Receptor Signaling Adaptor Proteins; 0/Environmental Pollutants; 0/Receptors, Tumor Necrosis Factor; 0/Zinc Compounds; 7487-94-7/Mercuric Chloride; 7646-85-7/zinc chloride

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Gentamicin-induced apoptosis in LLC-PK1 cells: involvement of lysosomes and mitochondria.
Next Document:  Mast cell mediators in citric acid-induced airway constriction of guinea pigs.